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Cardiovascular aging is characterized by increased thickness and stiffness of the central arterial walls, a preserved ejection fraction at rest through an increase in the thickness of the left ventricular wall, an enhanced ability of the myocardium to bear force in late systole, and diminished responsiveness to β-adrenergic modulation.During maximal exercise older individuals, as compared to younger individuals, exhibit diminished exercise capacity with preserved cardiac reserve, due to peripheral factors that determine oxygen utilization; lower ejection fraction due to an age-associated uncoupling of arterial and cardiac energies; and reduced cardiac output with preserved stroke volume, due to an age-associated decrease in maximal heart rate.The incidence and prevalence of cardiovascular diseases increase with advancing age. This association may be explained, in part, by the fact that many of the same factors that underlie the age-associated structural and functional alterations in central arterial walls are also implicated in the pathogenesis of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Single-gene disorders are caused by mutations of specific genes in the human genetic material.Polymorphic changes are variations in the genetic material that do not cause disease but may increase an individual's susceptibility to a particular disease.X-linked disorders are caused by an inheritance of a mutant gene found in the X chromosome.Common diseases of adults, such as coronary artery disease, hypertension, diabetes, and some congenital malformations, are not inherited as a single-gene disorder or a chromosomal abnormality. [ABSTRACT FROM AUTHOR]

Cardiovascular risk factors are commonly associated with erectile dysfunction and should be identified and treated.Patients with cardiovascular disease should be assessed and counseled regarding their fitness for sexual activity.Sexual activity is associated with a small risk (0.9% attributable risk) of an adverse cardiovascular event.The PDE-5 inhibitors, the most commonly prescribed treatment for erectile dysfunction, are effective and safe in most patients with stable cardiovascular disease.The PDE-5 inhibitors are absolutely contraindicated in patients receiving nitrates for cardiovascular disease or individuals using recreational amyl nitrite/nitrate ("poppers").Published recommendations such as the American College of Cardiology/American Heart Association (ACC/AHA) and Princeton Consensus Guidelines provide a logical approach to the management of patients with cardiovascular disease and erectile dysfunction. [ABSTRACT FROM AUTHOR]

The natural opiate (morphine) and the synthetic opioids have profound analgesic properties and are useful in high doses for the maintenance of cardiac patients because of the relatively benign effects of these agents on hemodynamics.Muscle relaxants are used to facilitate endotracheal intubation, to aid in surgical exposure, and to prevent patient movement during critical periods during surgery.Catheterization of central veins and arterial cannulation for pressure monitoring are almost universally done for cardiovascular surgery.The EEG is generally used to monitor brain activity and gross perfusion of the brain during cardiopulmonary bypass surgery.Intraoperative echocardiography is very helpful in evaluating mitral valve repair, and to aid in diagnosis of atheromatous plaques and dissection of the thoracic aorta. [ABSTRACT FROM AUTHOR]

Catheter ablation has become the first truly curative treatment for many supraventricular and some ventricular tachycardias.The success rate for anteroseptal and midseptal accessory pathways ranges between 95% and 100%, but the risk of creating a more complete atrioventricular (AV) block in patients with midseptal accessory pathways is not negligible. The recurrence rate after ablation of accessory pathways is low, and if necessary, the patient can be reablated with a high success rate. Patients should be followed for at least 6 months after ablation.Catheter ablation in patients with AV nodal reentrant tachycardia (AVNRT) has been very successful in curing patients.The success rate for catheter ablation for common atrial flutter ranges between 65% and 98%. There is a risk of recurrence of ablated atrial flutter of 10% to 55%.In general, catheter ablation for atrial tachycardia is effective and safe.In ablation procedures to treat atrial fibrillation, ostial pulmonary vein isolation is reported to result in a success rate of 70% to 80%. Potential complications include pulmonary vein stenosis and esophageal injury with or without atrioesophageal fistula.Atrioventricular nodal ablation followed by pacemaker implantation is limited to patents in whom catheter ablation cannot cure the supraventricular arrhythmia, such as left atrial flutter, multifocal atrial tachycardia, and some atrial fibrillation. It is an accepted modality in patients with atrial fibrillation with a very rapid ventricular response that cannot be controlled with antiarrhythmic medication, external and internal cardioversion, and perhaps the atrial implantable defibrillator.Catheter ablation of ventricular tachycardia (VT) is much more modest in its success as compared to results in patients with supraventricular tachycardias (SVTs). In idiopathic VT, however, catheter ablation is a curative technique and should be offered early in the treatment of symptomatic patients.Primary idiopathic ventricular fibrillation is characterized by dominant triggers from the distal Purkinje system. The triggers can be eliminated by focal energy delivery. [ABSTRACT FROM AUTHOR]

Death from cardiac causes is 10 to 20 times more common in patients with chronic renal failure than in age- and gender-matched individuals within the general population.Patients with decreased renal function do less well than those with normal renal function after acute coronary syndromes, including myocardial infarction, percutaneous coronary intervention, and coronary bypass surgery.Chronic kidney disease is an increasing public health problem in developed countries, due in part to greater prevalence of obesity and diabetes mellitus in populations that are living longer.Cohort studies have identified hypertension, diabetes, hyperlipidemia, obesity, and smoking as risk factors in the general population for the development of chronic kidney disease.Renal function is impaired in many patients with heart failure.Current management options for treatment of chronic kidney disease are based on the control of hypertension, proteinuria, hyperlipidemia, glucose, and smoking.Inhibition of the renin-angiotensin system is key to the preservation of glomerular function in chronic kidney disease, just as it is for cardiovascular function in heart failure. [ABSTRACT FROM AUTHOR]

Diabetes mellitus affects more than 150 million people worldwide, and the prevalence of the disease is on the increase.Cardiac death is increased up to threefold in men and up to fivefold in women with diabetes.Insulin resistance is one of the most important markers of the metabolic syndrome.There is a close link between inflammation and initiation/progression of atheroma formation.Insulin resistant states induce a generalized inflammatory state.Novel molecules that may link inflammation, insulin resistance, and atherosclerosis include leptin and adiponectin.Inflammation can predispose to thrombosis.The accumulation of advanced glycation end (AGE) products in diabetes impairs endothelial function, most likely by quenching nitric oxide. [ABSTRACT FROM AUTHOR]

Most of our standard therapies are cost-effective by the usual benchmarks.Cost-effectiveness analysis offers methods to help show that therapeutic choices provide good value.Cost-effectiveness analysis can help both in medical decision making and in informing public policy. [ABSTRACT FROM AUTHOR]

Even successfully revascularized hearts undergo ventricular remodeling, a process of neurohormonal imbalance and apoptosis that leads to ischemic heart failure. Until recently, cardiologists believed that ventricular remodeling was irreversible and that the heart had no capacity for self-renewal. It now appears that the injured heart may be repaired by resident cardiac stem cells and by stem cells that originate from bone marrow.Stem cells have a capacity for self-renewal and can sustain, generate, and replace any terminally differentiated cell in the body. The adult bone marrow is a reservoir of stem cells that have enormous plasticity. By promoting angiogenesis, stem cell therapy may improve left ventricular function or relieve angina in patients with acute or chronic coronary artery disease.At present, research and clinical interest is largely devoted to skeletal myoblasts and autologous bone-marrow mononuclear cells (ABMMNCs).Skeletal myoblasts offer myocyte replacement therapy for scarred myocardial segments, and ABMMNCs offer neoangiogenesis and regenerative therapy for acute and chronic ischemic heart disease involving viable myocardial tissue.Early clinical trials using these cells have yielded promising initial results regarding safety and efficacy.Stem cells may be delivered through coronary arteries, through coronary veins, or by means of peripheral-vein infusion. Alternatively, direct intramyocardial injection may be performed, utilizing a surgical, transendocardial, or transvenous approach. Also, a delivery strategy may involve mobilization of stem cells from the bone marrow by means of cytokine therapy, with or without peripheral harvesting.Intracoronary infusion is the most widely used cell delivery method in the clinical setting, especially after an acute myocardial infarction (AMI). Stem cells delivered 4 to 9 days after an AMI have been associated with a good safety profile. The technique is similar to that used for coronary angioplasty.Intramyocardial injection is the preferred delivery route in patients with chronic total occlusion of coronary arteries or chronic congestive heart failure. Intramyocardial injection can be performed as a transepicardial, transendocardial, or transcoronary venous injection.The transendocardial route allows therapy to be precisely targeted. Targeted therapy is gaining importance as the ineffectiveness of injecting ABMMNCs into scar tissue becomes increasingly evident.Skeletal myoblast therapy is used for ischemic heart failure with areas of nonviable myocardium or scar tissue and compromised systolic left ventricular function.The recent release of the 1-year results of the TOPCAREAMI trial confirmed the overall safety of stem cell therapy after an AMI. Although ventricular arrhythmias are a potential concern with skeletal myoblasts, this complication has not been observed with ABMMNCs. Nevertheless, the latter cells may cause accelerated atherogenesis or myocardial calcification.Investigations are underway at the molecular level to elucidate the mechanisms of stem cell therapy, which are attributed to transdifferentiation versus cell fusion. In animal models of ischemic heart disease, stem cell therapy appears to increase neovascularization.Clinically, the next step in cardiac cell therapy is to answer basic questions, such as whom should be treated, when treatment should be initiated, and what products are ideal in each clinical scenario. [ABSTRACT FROM AUTHOR]

Most common cardiovascular disorders, including atherosclerosis, heart failure, hypertension, and arrhythmias, are multigenic or complex disorders.Dilated cardiomyopathies are most commonly associated with mutations of the cytoskeletal proteins, including dystrophin complex that binds cell cytoskeleton to the extracellular matrix, such as desmin, etc.The long QT syndromes can be subclassified based on genotypes, such that IKs (the slowly activating delayed rectifier potassium current) potassium channel mutations account for the majority of LQT1/5 and the JLN1/2 phenotypes. The IKr (the rapidly activating delayed rectifier potassium current) potassium channel mutations may account for the LQT2/6 syndromes and the sodium channel mutations account for LQT3.Some candidate genes for susceptibility to myocardial infarction include thrombospondin-1,4, lymphotoxin-α, and 5-lipoxygenase, but others are being reported presently.Single nucleotide polymorphism (SNP) variations are being linked to cardiovascular disease, including the apolipoprotein E-ɛ4 4 polymorphism, which predisposes individuals to coronary artery disease, and variations in the β2-adrenergic receptor polymorphism, which predispose individuals to heart failure. [ABSTRACT FROM AUTHOR]

The field of cardiovascular gene therapy has undergone dramatic changes since its inception 15 years ago.1,2 The field began with development of basic techniques for introducing recombinant genes (gene transfer) into cells of the vasculature and the heart. Viral and nonviral vectors were designed and demonstrated to facilitate gene transfer and gene expression. These vectors were shown to be effective in animal models of cardiovascular disease. Within the past 10 years, there has been a rapid expansion of translation of the basic science and preclinical principles to all phases of clinical investigation. Results of these studies have begun to document the feasibility, safety, and promise of human gene transfer for cardiovascular disease. [ABSTRACT FROM AUTHOR]

At any given level of effort, the cardiac workload is greater in obese subjects.Left ventricular hypertrophy occurs with morbid obesity and may be associated with left ventricular diastolic dysfunction.With increasing rates of obesity, type 2 diabetes and the metabolic syndrome are seen in childhood.The metabolic syndrome and inflammation are associated.Genetic factors play an important role in obesity.Obesity is strongly associated with systemic arterial hypertension.There is an increased stroke risk with obesity.Obesity is strongly associated with systemic arterial hypertension.Morbid obesity is an independent risk factor for death after pulmonary embolism.Obesity is a classical cause of alveolar hypoventilation. [ABSTRACT FROM AUTHOR]

Serum cholesterol, which normally consists predominantly of low-density lipoprotein (LDL) cholesterol (LDLC), is influenced by the liver's expression of LDL receptors; the latter is regulated by the cholesterol content of liver cells.The process whereby cholesterol passes from peripheral tissues through high-density lipoprotein (HDL) and back to the liver is called reverse cholesterol transport.Cumulative data suggest that the risk of coronary heart disease declines to a total serum cholesterol of 150 mg/dL corresponding to an LDL level of 100 mg/dL or less. Highrisk coronary heart disease patients benefit from even lower LDL serum values—down to values of 70 mg/dL or less. The concept has emerged now that "the lower, the better" for risk reduction with LDL-C levels.Each component of atherogenic dyslipidemia appears to be independently atherogenic.In patients with elevated triglycerides, the non-HDL cholesterol (HDL-C) level is a better indicator of the total apo-B containing lipoproteins than is the LDL-C.Centrally important in atherosclerotic cardiovascular disease (ASCVD) risk reduction are complete smoking cessation, reduction of LDL-C, weight loss, and increased physical activity.Statins are the leader in LDL-lowering drugs and are generally well tolerated. They should not be given to patients with underlying liver disease. They diminish cholesterol synthesis by the liver.Ezetemide inhibits cholesterol absorption from the bowel. When combined with a statin, the LDL-lowering effect is enhanced. For every lowering of LDL-C by 1%, there is an approximate 1% reduction in major coronary events.Statin therapy is just as effective for reducing risk for ASCVD when diabetes is present as when it is not.Prospective studies have shown that an abnormal anklebrachial index (ABI) identifies an increased risk for future coronary events; that is, most patients with peripheral vascular disease also have important coronary heart disease.The metabolic syndrome includes any three of the following five conditions: 1.Elevated fasting glucose of 100 mg/dL or above2.Elevated blood pressure of at least 130 mm Hg systolic or at least 85 mm Hg diastolic3.Reduced HDL cholesterol (< 40 mg/dL in men and <50 mg/dL in women)4.Elevated serum triglyceride level of at least 150 mg/dL5.Abdominal obesity, that is, waist circumference of over 102 cm/40″ in men or over 88 cm/34.5″ in womenThe metabolic syndrome has an increased risk of ASCVD and for type II diabetes.A proinflammatory state predisposes to major cardiovascular events. [ABSTRACT FROM AUTHOR]

Smoking is the leading cause of preventable cardiovascular disease (CVD). Epidemiologic and biologic evidence consistently demonstrates that smokers have an increased risk of CVD compared to nonsmokers. Both cardiac and extracardiac CVDs are more prevalent among smokers.Secondhand smoke is an important cause of CVD in nonsmokers. Secondhand smoke increases the risk of CVD by at least 30%, and given that a large part of the population is still breathing secondhand smoke, it is vital to counsel patients to avoid secondhand smoke exposure.The effects of tobacco smoke on the cardiovascular system accrue over a short period of time and are synergistic with other established cardiovascular risk factors. Tobacco smoke affects the cardiovascular system within minutes of exposure. Smokers and nonsmokers should be aware of this fact. Smokers should be encouraged to quit, and nonsmokers should fight for smoke-free environments.Every smoker should be encouraged to quit and every patient should be informed about the harmful effects of secondhand smoke (SHS) exposure. Smoking cessation has been proven to decrease mortality, regardless of age at quitting or disease stage. Several pharmacologic agents are now available to help patients quit. Pharmacotherapy is more likely to be effective if complemented with behavioral counseling. Secondhand smoke counseling will increase the likelihood of quitting for a smoker and encourage nonsmokers to advocate for smoke-free environments. At the very least, physicians should refer smokers to a quit line. Options should be discussed with the patient and behavioral treatment should be encouraged as it increases the likelihood of success. Smoking cessation is also effective in reducing CVD mortality. The excess risk of myocardial infarction (MI) is reduced by 50% within 1 year of quitting.Physicians should become tobacco control activists. A comprehensive tobacco control program, that includes taxation, smoke-free environments, and exposing the tobacco industry, has been shown to be effective in decreasing smoking prevalence and cardiovascular disease mortality. Physicians should become actively involved in the fight against tobacco.The mechanisms by which tobacco smoke leads to CVD include platelet activation, endothelial dysfunction, inflammation, altered lipid levels and metabolism, and hemodynamic effects. These effects interact with each other and are synergistic with other established CVD risk factors (e.g., obesity, diabetes). Some of these effects occur soon after exposure has happened; as little as half an hour of SHS exposure leads to platelet and endothelial dysfunction.A comprehensive tobacco control program reduces CVD mortality. Smoke-free environments are among the most effective measures to reduce CVD mortality. In addition to protecting nonsmokers from secondhand smoke, these environments make it easier for smokers to cut down or quit. Physicians should become active tobacco control advocates. [ABSTRACT FROM AUTHOR]

Both occupation and recreational exercise can reduce cardiovascular events by up to one half.Diverse forms of exercise, including walking, and even exercise begun later in life improve cardiovascular outcomes.Current guideline recommendations are for 30 minutes of moderate-intensity exercise on at least 3 days, preferably all days of the week for all adults.The overall reduction in cardiovascular events with exercise training is far greater than the increased risk of events that occur during exercise.Cardiac rehabilitation is an individualized, multidisciplinary, comprehensive approach to cardiovascular risk reduction that can result in a 25% reduction in overall mortality.Cardiac rehabilitation begins during the initial hospitalization, should be continued early after discharge, and should promote lifelong adherence to lifestyle changes.Enhanced endothelial function is a major mechanism for the improved myocardial perfusion and reduction in ischemia observed with exercise.The improved balance of parasympathetic to sympathetic tone greatly contributes to the reduction in sudden death seen with exercise.Long-term outcomes of exercise training include beneficial effects on several traditional cardiovascular risk factors and reduction in the progression of atherosclerosis. [ABSTRACT FROM AUTHOR]

Epidemiologic studies have identified hundreds of risk factors and risk markers for development of cardiovascular disease (CVD) and coronary heart disease (CHD).The established risk factors for CVD include dyslipidemia, hypertension, cigarette smoking, obesity, diabetes and impaired fasting glucose, and family history of premature CVD.Each of the measured risk factors confers risk in a continuous, graded fashion, with no clear threshold levels above which risk increases sharply, or below which risk is absent. Each of the established risk factors is associated with increased risk for CVD independent of the others.However, consideration of each risk factor in isolation is insufficient to classify an individual's global CVD risk. Each risk factor is associated with markedly elevated levels of risk when placed in the context of greater burden of other risk factors.Multivariable risk formulas, such as the Framingham risk score, have been developed to assist in estimating an individual's absolute risk for CHD over 10 years, in order to guide treatment decisions for primary prevention of CVD. For younger individuals, in whom 10-year risks are likely to be low, consideration should be given to the absolute lifetime risk for CVD. The intensity of preventive therapy should match the level of estimated absolute risk.Risk factors often occur together, or cluster, within individuals. This is particularly seen in individuals with the metabolic syndrome, a complex syndrome involving increased visceral adiposity, insulin resistance, dyslipidemia with high triglycerides and low high-density lipoprotein (HDL) cholesterol, elevated blood pressure, and elevations in inflammatory and prothrombotic markers.Multiple newer risk markers have been identified that are associated with CVD risk independent of the established risk factors. Whereas these newer risk markers provide important insights into the process of atherogenesis, none has yet proven to be worthy of routine screening and treatment.Effective prevention of CVD requires more intensive lifestyle modification at the population and individual level and at younger ages, greater recognition of the concept of global CVD risk, and more aggressive preventive efforts, especially among elderly individuals, who are at highest risk. [ABSTRACT FROM AUTHOR]

Congenital heart disease is estimated to affect 4 in 1000 to 8 in 1000 live births in the United States.Down syndrome (trisomy 21) is the most common chromosomal disorder; it occurs in approximately 1 in 800 births and the incidence rises steeply for women older than 35 years. Complete atrioventricular canal abnormalities account for 60% of heart defects in these patients.Coarctation of the aorta is the most common cardiovascular defect in patients with Turner syndrome.Patients with DiGeorge syndrome often have conotruncal abnormalities, including tetralogy of Fallot, ventricular septal defect (VSD), truncus arteriosus, and aortic arch anomalies.Holt-Oram syndrome has anomalies of the upper limbs and heart, including secundum atrial septal defects (ASDs).The most common cardiac abnormality with Noonan syndrome is valvular pulmonic stenosis. [ABSTRACT FROM AUTHOR]

Several arrhythmia syndromes that for long were considered idiopathic are now known to have a genetic basis and are caused by mutations in genes primarily encoding ion channels.Mutations in cardiac ion channels lead to abnormal ionic current characteristics via mechanisms, such as defective channel gating or reduction in sarcolemmal channel expression. This results in the electrocardiogram (ECG) features or arrhythmogenesis in the inherited arrhythmia syndromes.The genetic basis for most arrhythmia syndromes is heterogeneous (a given disorder may be caused by mutations in different genes) and evidence for further genetic heterogeneity exists.It is becoming increasingly clear that therapy should take the type of gene affected into consideration (gene-specific therapy).Considerable heterogeneity may exist in disease manifestation (both in severity as well as differences in disease features) among family members carrying the same mutation. [ABSTRACT FROM AUTHOR]

Emery-Dreifuss muscular dystrophy is a rare X-linked recessive disease manifested by early contracture, progressive muscle wasting, and cardiomyopathy with cardiac arrhythmias. Males are primarily affected.Hypertrophic cardiomyopathy is an autosomal dominant inherited disease caused mostly by mutations in sarcomeric proteins, notably the heavy chain of myosin, a tropomyosin, and cardiac troponin T.Duchenne's muscular dystrophy is an X-linked recessive myopathy of childhood caused by mutation of the dystrophia gene. Weakness beginning within the first 5 years of life progresses to the loss of ability to walk independently by early in the second decade and often death by the third decade. Serum creatine kinase (CK) levels are markedly elevated early in life. Cardiac involvement leads to congestive heart failure (CHF), and patients also have restrictive pulmonary disease.Myotonic dystrophy is the most common adult-onset myopathy and is inherited as autosomal dominant and is characterized by progressive muscle weakness, cardiomyopathy, delayed muscle relaxation, cataracts, frontal balding, diabetes mellitus, and male infertility. [ABSTRACT FROM AUTHOR]

Marfan syndrome is an autosomal dominant disease characterized by pleiotropic manifestations involving the cardiovascular, ocular, and skeletal systems. The most common cardiovascular complication in patients with Marfan syndrome is progressive aortic root enlargement initially occurring at the sinuses of Valsalva. Some patients have dissections of the aorta, most often a type I dissection. Mitral valve prolapse is very common in these patients.The majority of patients with thoracic aortic aneurysms and dissections who have cystic medial necrosis of the aorta do not have Marfan syndrome.Ehlers-Danlos syndrome (EDS) is a heterogeneous group of disorders that are classified together on the basis of skin hyperextensibility, cutaneous fragility, joint laxity, dystrophic scarring, and easy bruising. Spontaneous arterial rupture occurs in type IV EDS.Supravalvular aortic stenosis is an autosomal dominant disorder caused by narrowing of the ascending aorta just distal to the coronary ostia.Pseudoxanthoma elasticum is an inherited disease caused by progressive calcification of elastic fibers in the connective tissue throughout the body. [ABSTRACT FROM AUTHOR]

The combination of V5 with another lead (II, III, V4, or V6) increases the sensitivity of ischemia detection to 90%.In high-risk patients, most intraoperative ST segment changes occur in the absence of major hemodynamic lability, and maintenance of hemodynamic variables (blood pressure and heart rate) to within 20% of baseline values does not appear to reduce intraoperative ischemic events.Electrocardiograph (ECG) monitoring for myocardial ischemia augmented by continuous, computerized ECG monitors should be continued into the early postoperative period for high-risk patients.Invasive blood pressure monitoring is indicated when (1) large or abrupt hemodynamic changes are anticipated intraoperatively, (2) coexisting disease necessitates close hemodynamic management, (3) pharmacologic or mechanical intervention is anticipated or planned, or (4) noninvasive methods are impractical or impossible.Excessive variation of the systolic blood pressure (>15 mm Hg) is a strong predictor of occult hypovolemia.Overall, the risk of an ischemic complication from peripheral arterial catheterization is less than 0.1%.Central venous pressure (CVP) reflects the balance among intravascular volume, venous tone, and right ventricular function.In general, a single isolated CVP value provides little information unless it is very high or very low.Recent development of small, portable ultrasound machines has made it possible to image the great veins of the neck prior to or during placement of central venous catheters. This has been shown in multiple clinical studies as well as in a recent meta-analysis to decrease the incidence of failed catheter placement as well as the complication rate, especially in high-risk patients.Pulmonary artery catheter (PAC)-derived filling pressures are a poor index of right and left ventricular preload as they are influenced by heart rate, valvular disease, myocardial compliance, myocardial ischemia, and positive pressure ventilation.Perioperative goal-directed therapy, that is, the "optimization" of oxygen delivery and cardiac index, has been shown to reduce mortality, complications, and hospital length of stay in high-risk surgical patients.According to current American Society of Anesthesiologists (ASA) recommendations, the use of PAC is considered necessary only in high-risk patients undergoing high-risk surgery, and under the condition that the practice environment is favorable (i.e., knowledgeable and experienced physicians and intensive care unit nurses).Mixed venous oxygen saturation depends on the balance between oxygen delivery and consumption, and might be one of the more telling indices for judging the adequacy of the patient's hemodynamic status.Thermodilution is the standard method for measuring cardiac output; it is subject, however, to intrinsic variability, effect of intracardiac shunts and right-sided valvular regurgitation, and influence of other factors affecting instantaneous blood temperature.Two newer cardiac output measurement methods that obviate the need for a PAC include the transpulmonary arterial thermodilution and the lithium dilution. Both seem to offer accuracy similar to the traditional thermodilution method.Several methods exist for continuous measurement of cardiac output. The first method employs a modified PAC with a blood-warming filament. It does not produce true real-time continuous measurements, but rather a trend of recent measurements over a couple of minutes.Esophageal Doppler cardiac output (CO) measurement employs a probe inserted into the lower esophagus to measure descending aorta blood flow. It tends to underestimate CO measured by other methods, although accurately tracking changes occurring over time.… [ABSTRACT FROM AUTHOR]

The autonomic nervous system, especially through the cranial parasympathetic and lumbosacral sympathetic outflow, is closely involved in the beat-to-beat control of systemic blood pressure, heart rate, and the regional blood supply to skeletal muscle and vital organs. It is of major importance in ensuring adequate tissue perfusion, in maintaining supplies of oxygen and nutrients, and in transporting metabolic end-products in response to the demands of varying situations. It accomplishes these actions through a complex system of pathways that involves the brain and spinal cord, preganglionic and postganglionic pathways, and synapses at the target organs; the immense flexibility and capability of the autonomic nervous system are dependent on intricate pathways that may be damaged in a variety of conditions that affect one or more sites with the brain, spinal cord, or periphery1 (Fig. 88.1). A key component is the baroreflex pathway, an exquisitely sensitive mechanism that provides beat-bybeat blood pressure control (Fig. 88.2). This chapter discusses the classification of autonomic disorders that affect the cardiovascular system, and describes the main clinical manifestations, tests of autonomic dysfunction, and features of key major autonomic disorders. [ABSTRACT FROM AUTHOR]

Patient evaluation should be the same in the preoperative setting as in any other setting. To date, no tests or interventions have been shown to be of benefit to patients in the preoperative setting that are not likewise of benefit to patients in the nonpreoperative setting. For this reason, guidelines suggest that the clinical evaluation and testing for patients in the preoperative setting conform to that which would be pursued in the nonpreoperative setting.Noninvasive testing should be pursued selectively. Following bayesian logic, noninvasive testing, like all medical tests, will be of most use, and provide the most information, for patients at indeterminate or intermediate risk. Those patients at highest clinical risk and lowest clinical risk are unlikely to have their status or treatment changed by noninvasive testing.Perioperative beta-blocker therapy improves outcomes in high-risk patients. Studies to date suggest that patients at high clinical risk, or having abnormal noninvasive testing, will benefit from perioperative beta-blockade. The role for beta-blocker therapy during surgery for low risk patients is less clear.Prior coronary revascularization in the recent past is associated with low perioperative cardiac risk during noncardiac surgery. Numerous studies suggest that patients who have undergone coronary artery bypass grafting or percutaneous coronary revascularization, and are without symptoms of active coronary artery disease, have a very low risk of perioperative cardiac events. Data suggest that this benefit extends up to 5 years after coronary artery bypass surgery.Preoperative evaluation offers a unique opportunity to improve modifiable cardiac risk factors. Cardiovascular disease and its complications are the leading cause of death in the developed world. Even patients at low risk for perioperative cardiac complications still face the significant likelihood of eventually developing, and dying from, cardiovascular disease. It is important to exploit the opportunity to address the modifiable risk factors.Surgical treatment of valvular disease carries the same indications prior to noncardiac surgery. Patients presenting for evaluation prior to noncardiac surgery should undergo aortic or mitral valve surgery only if the valve surgery is indicated according to the American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for treatment of valvular disease.Percutaneous coronary revascularization should be pursued in accordance with the AHA/ACC guidelines. Current data suggest no reduction in perioperative mortality by the pursuit of preoperative coronary revascularization for that reason. Therefore, the mere presence of coronary lesions does not indicate percutaneous revascularization. Revascularization should be pursued for longterm benefit, according to the ACC/AHA guidelines, as for any other patient.Patient functional capacity is important to determine perioperative risk. Patient exercise tolerance affects risk for perioperative events significantly. A clinical assessment of each patient's exercise capacity informs the determination of the presence of angina, and also directly relates to the patient's perioperative risk. [ABSTRACT FROM AUTHOR]

Neuromuscular disorders and skeletal myopathies comprise a very heterogeneous and somewhat rare group of disorders that often involves multiple organs and have overlapping clinical manifestations.The molecular genetic basis of many neuromuscular disorders and skeletal myopathies have been delineated during the past two decades, providing insight into the pathogenesis of these disorders and raising the possibility of preclinical diagnosis, risk stratification, and specific therapies.The heart is commonly involved in neuromuscular disorders and skeletal myopathies.Cardiac involvement is often subclinical. Hence, routine systematic cardiac evaluation is warranted in all patients with neuromuscular disorders and skeletal myopathies.Cardiac involvement typically manifests as dilated cardiomyopathy with congestive heart failure.Cardiac conduction defects involving sinoatrial (SA) and atrioventricular (AV) nodes and bundle branches are common and progressive, particularly in neuromuscular disorders such as myotonic dystrophy and muscular dystrophies, often requiring permanent pacemaker implantation.Cardiac hypertrophy is present in a significant number of patients with neuromuscular disorders, such as Friedreich ataxia and often mimics hypertrophic cardiomyopathy (phenocopy).Cardiac involvement is the major cause of morbidity and mortality in patients with neuromuscular disorders and skeletal myopathies. [ABSTRACT FROM AUTHOR]

The term hypercoagulable states is used interchangeably with thrombophilia or prethrombotic state to refer to hereditary or acquired conditions that predispose individuals to thrombosis.The coagulation system, also known as the coagulation cascade, is a highly coordinated and tightly linked series of enzymatic reactions, involving the sequential conversion of plasma clotting factors that circulate in their inactive zymogen forms to enzymatically active serine proteases, culminating in the formation of fibrin.The coagulation system is normally kept in check by several physiological anticoagulant (antithrombotic) mechanisms. These include antithrombin III, the protein C/protein S/thrombomodulin system, tissue factor pathway inhibitor, the protein Z/protein Z-dependent protease inhibitor system, and the fibrinolytic system.Primary hypercoagulable states are mostly inherited thrombophilias caused by (1) quantitative deficiencies or qualitative defects of the physiologic anticoagulants, or (2) increased levels or function of the coagulation factors.Secondary hypercoagulable states encompass a variety of diseases and conditions, most of which are acquired, which predispose individuals to thrombosis by complex and multifactorial mechanisms.In gene-gene interactions, the inheritance of more than one thrombophilic defect leads to an increased lifelong risk of thrombosis.In gene-environment interactions, many thrombotic complications in individuals with inherited (primary) hypercoagulable states are precipitated by acquired, acute thrombogenic insults, pointing to complex interactions between genetic and environmental factors in the pathogenesis of clinical thrombotic events.The hypercoagulable workup is a laboratory evaluation of individuals with suspected hypercoagulable states. It is guided by the history, physical examination, and implications for management decisions. [ABSTRACT FROM AUTHOR]

The prevalence of heart disease in women is approximately 1% with an overall complication rate of 13% to 18%.Congenital heart disease accounts for more than 50% of pregnant patients with heart disease.The patients at highest risk are those with critical aortic stenosis (AS), Marfan's syndrome with an aortic diameter of 40 mm or more, cyanotic heart disease, pulmonary hypertension, mechanical prostheses, or severe left ventricle (LV) dysfunction.Suggested guidelines for safety of pregnancy in patients with cyanotic congenital heart disease include maternal functional status, O2 saturation of 85% to 90% or more, hemoglobin of 16 g/dL or more, pulmonary artery to systemic blood pressure ratio of 70% or more, and a left ventricular ejection fraction (EF) of 35% to 40% or less.Women who have significant ventricular dysfunction (New York Heart Association class III or IV) have a poor prognosis in pregnancy. Pregnancy should be discouraged when the EF is less than 25%.Hypertension affects as many as 10% of all pregnancies and remains a major cause of maternal and fetal morbidity and mortality.Half of the aortic dissections that develop in women younger than 40 years of age occur in association with pregnancy.Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II blockers are contraindicated in pregnancy. [ABSTRACT FROM AUTHOR]

Severe anemia is an important problem in patients with underlying coronary heart disease because further reduction in oxygen delivery to myocardium supplied by stenotic coronary arteries may lead to angina or myocardial infarction.Cautious transfusion may be critically important acutely in the patient with an acute coronary syndrome.Increases in fetal hemoglobin levels may reduce the frequency of sickle cell crisis spells in the adult.Congenital heart disease with right-to-left shunting is associated with the development of erythrocytosis. The need for and frequency of phlebotomy should be dictated by the patient's symptoms or by the erythropoietin level as a measure of tissue hypoxia.Clinical problems related to primary thrombocythemia occur with platelet counts in excess of 700,000 mm3 and include both hemorrhagic and thrombotic events.Prolonged cardiopulmonary bypass is often associated with abnormalities in coagulation and hemolytic anemia.Mutations in the factor V or prothrombin gene may lead to a hypercoagulable state. [ABSTRACT FROM AUTHOR]

Shock is a syndrome in which an acute deficiency of vital tissue perfusion due to hemodynamic dysfunction leads to progressive metabolic and functional deterioration that, if not reversed, will lead to death. The common feature of shock is that cardiac output is inadequate to perfuse all the organs with sufficient blood to maintain tissue integrity. This inadequacy of perfusion is usually but not always accompanied by hypotension and intense regional vasoconstriction. The perfusion deficit may result in a cascade of further complications, such as the release of vasodilator factors that increase capillary permeability and may further lower blood pressure, leading ultimately to cardiac dysrhythmias and death. Shock can result from both cardiovascular and noncardiovascular illnesses (Table 87.1). Cardiac causes are the focus of concern for the cardiologist, and it is critical to exclude noncardiac causes before launching into aggressive cardiovascular therapy. [ABSTRACT FROM AUTHOR]

Substance abuse was common in Sir Arthur Conan Doyle's time, and it remains a major problem today. It has been estimated that 6.9% of the U.S. population are illicit drug users.1 The effects of substance abuse on the cardiovascular system can be divided into two broad categories: (1) general effects of substance abuse, such as endocarditis or vasculitis in intravenous drug abusers; and (2) specific cardiovascular toxicity associated with specific drugs. Endocarditis in drug abusers has been discussed in detail in Chapter 19. Thus, this chapter focuses on cardiovascular manifestations of specific drugs, particularly cocaine and ethanol. Tobacco abuse, which constitutes a major cause of cardiovascular morbidity and mortality due to premature coronary atherosclerosis, is discussed in Chapter 127. [ABSTRACT FROM AUTHOR]

From the very beginning of the epidemic of human immunodeficiency virus (HIV) infection, which surfaced in the late 1970s, involvement of the heart was described in autopsies of patients who had died of the acquired immune deficiency syndrome (AIDS). The early reports described Kaposi's sarcoma involving the myocardium and pericardium,1,2 often as incidental findings at autopsy. Large series of patients with AIDS described nonbacterial thrombotic endocarditis, a possibly nonspecific finding resulting from the severe cachexia and wasting frequently seen with this disease.3,4 Later, larger autopsy series showed frequent evidence of focal pockets of inflammatory cells in the myocardium, at times with incidental findings of fungal or parasitic involvement of the myocardium, but clinical manifestations of this myocardial involvement were unusual. Rarely, severe myocarditis due to toxoplasmosis was seen as a cause of death. [ABSTRACT FROM AUTHOR]

Increased mortality from cardiovascular disease among adults with hypopituitarism is perhaps related to growth hormone deficiency.Major cardiovascular manifestations of acromegaly include cardiomegaly, cardiac hypertrophy, hypertension, congestive heart failure, coronary artery disease, and arrhythmias.The excess mortality of acromegaly is abolished by successful treatment of acromegaly.The major cardiovascular manifestation of adrenal insufficiency is arterial hypotension.Major cardiovascular manifestations of Cushing's syndrome include hypertension, myocardial hypertrophy, and a prothrombotic state.The major cardiovascular manifestation of mineralocorticoid excess is hypertension, more common than previously thought.Hypokalemia is important in mineralocorticoid disorders, but most patients are normokalemic.Treatment with mineralocorticoid antagonist is beneficial following myocardial infarction and in congestive heart failure.The major cardiovascular manifestation of pheochromocytoma is hypertension.In pheochromocytoma, prompt treatment is important.Metabolic syndrome is important as a risk factor for the development of atherosclerotic disease and type 2 diabetes mellitus.The increased cardiovascular mortality in diabetes mellitus is reduced by aggressive treatment of multiple risk factors.Intensive treatment of hyperglycemia reduces mortality in critical illness.There is excess cardiovascular mortality in primary hyperparathyroidism.The "euthyroid sick syndrome" results from nonthyroidal illness.Major cardiovascular manifestations of hypothyroidism include bradycardia, cardiac enlargement, hypertension, low voltage on the ECG, and sometimes pericardial effusion."Subclinical hypothyroidism" is associated with in-creased lipids, but not yet conclusively linked to excess cardiovascular events.Major cardiovascular manifestations of hyperthyroidism include tachycardia and tachyarrhythmias, atrial fibrillation, increased pulse pressure, and increased cardiac contractility with decreased reserve.Overt and "subclinical" hyperthyroidism are linked to atrial fibrillation.Major cardiovascular manifestations of carcinoid syndrome include tricuspid regurgitation and pulmonic valve damage related to right-sided endocardial plaques.In carcinoid syndrome, there is increased morbidity and mortality in patients with carcinoid heart disease. [ABSTRACT FROM AUTHOR]

Many of the multisystem inflammato Interry connective tissue disorders promote or are linked to increased risk of atherosclerosis and its sequelae.Systemic lupus erythematosus patients often have verrucous endocarditis or valvular thickening with regurgitation or stenosis.Patients with antiphospholipid antibodies may develop spontaneous venous or arterial thromboses. [ABSTRACT FROM AUTHOR]

Three distinct disorders combine to produce chronic obstructive pulmonary disease (COPD): emphysema, peripheral airway disease or bronchospasm, and chronic bronchitis.Chronic obstructive pulmonary disease is defined as a disease state characterized by airflow limitation that is not fully reversible.Cigarette smoking is the major cause of COPD in both men and women in the United States.The most important familial factor associated with COPD is α1-antiprotease deficiency (i.e., α1-antitrypsin deficiency).With exercise, the arterial PO2 may rise minimally or fall in patients with COPD.The pulmonary function testing remains the standard in the initial evaluation of patients with COPD.In COPD, the forced expiratory volume (FEV), and maximal expiratory flow at 50% and 75% of vital capacity are reduced.Smoking cessation is the first and most important clinical intervention.Long-term oxygen therapy prolongs survival in selected patients with COPD.Lung transplantation therapy with a single lung is feasible in patients with COPD. [ABSTRACT FROM AUTHOR]

Tumors of the heart are uncommon, and they present in diverse and challenging ways. The heart may be the site of a primary tumor or may be invaded secondarily by malignancies that arise in adjacent or remote organs.Tumors—more frequently carcinomas than sarcomas—that involve the heart, pericardium, or both, originate as primary tumors in some other organ 20 to 40 times more often than they originate as primary tumors of the heart.Although less common than secondary tumors, primary tumors of the heart are far more challenging to both the cardiologist and the surgeon. These tumors usually present as intracavitary lesions. Although more than 75% of them are benign, clinical manifestations are common.Intracardiac myxomas are the most common benign tumors of the heart, constituting nearly 50% of all such tumors.Most patients with cardiac myxomas present with one or more effects of a triad of constitutional, embolic, and obstructive manifestations.Systemic tumor embolization occurs in 40% to 50% of patients with left atrial myxomas. Tumor fragments or surface clots most commonly embolize to arteries in the brain, kidneys, and extremities.Histologic examination of emboli recovered from a peripheral artery at operation can lead to diagnosis of an otherwise unsuspected intracardiac myxoma.Tumor embolization to the central nervous system constitutes about half of all embolic events caused by left atrial myxomas.Rhabdomyomas are the most frequent cardiac tumors in infants and children (usually males). These lesions usually present early in life and cause a variety of manifestations, including arrhythmias and sudden death.Lipomatous hypertrophy of the atrial septum is an unencapsulated hyperplasia of adipose tissue and may not represent a true tumor.Caseous mitral annular calcification is a more recently recognized unusual variant of mitral annular calcification that is generally clinically benign. However, its striking incidental appearance on echocardiography can lead to mistaken diagnosis of a tumor or an abscess.Mesotheliomas (lymphangioepitheliomas) of the atrioventricular node are the smallest tumors capable of producing sudden death by causing complete heart block.Recurrent, nonbloody pericardial effusion is common in children with a teratoma of the pericardium.For metastatic lesions, no particular type of malignant tumor predominates except possibly malignant melanoma, which involves the myocardium in more than 50% of cases. [ABSTRACT FROM AUTHOR]

Hypertension is a common disease that contributes importantly to the high cardiovascular morbidity and mortality observed in industrialized countries. The proper diagnosis and management of this disorder affords considerable reduction of the risk of developing cardiac, cerebral, and renal complications. Approximately 95% of patients with high blood pressure exhibit the so-called essential or primary form of hypertension. Various mechanisms are involved in the pathogenesis of this type of hypertension. This heterogeneity accounts for the diverse therapeutic approaches that have been utilized and for the rationale for individualizing treatment programs. In a small fraction of patients, the elevation of blood pressure is due to a specific cause (secondary hypertension). The recognition of such patients has improved markedly in recent years. This is relevant since secondary hypertension can often be cured by appropriate interventions. [ABSTRACT FROM AUTHOR]

The management of chronic heart failure has two goals. One is to produce short-term relief of symptoms and improvement in quality of life. The other is to slow or halt the progressive process of cardiac and peripheral dysfunction in heart failure that leads to long-term disability and shortened life expectancy. The former strategy is confined to patients with symptoms of heart failure; this may include exertional intolerance, shortness of breath or orthopnea, peripheral edema, or fatigue. It is important to recognize that not all heart failure is accompanied by congestive symptoms. Furthermore, some symptoms of heart failure may be subtle, leading to a reduced quality of life without the usual overt manifestations of heart failure. Therapy aimed at slowing progression of the disease is applicable in patients without symptoms as well as in those with symptoms. Left ventricular (LV) dysfunction may long antedate overt symptoms of heart failure, and the progressive nature of this LV dysfunction can potentially be prevented by aggressive therapeutic efforts. Indeed, treatment of heart failure symptoms must be accompanied by aggressive attempts to prevent progression of the disease, because the presence of symptoms identifies a patient whose condition is likely to progress in the absence of aggressive intervention. We therefore divide the therapeutic approaches for heart failure into these two separate categories. [ABSTRACT FROM AUTHOR]

The first description of the circulation of blood through the lungs has been attributed to Ibn Nafis (1210-1288).1 The concept was rediscovered by Michael Servetus, a Spanish physician during the Renaissance (1511-1553) and recorded, oddly enough, in two pages of his religious treatise, Christianismi Restitutio (1553).2 The definitive exposition of the pulmonary circulation was made by William Harvey in DeMotu Cordis (1628).3 The first observation of the pulmonary capillaries was first reported by Marcellus Malpighi (1661).4 Heart catheterization in humans, driven by a desire to obtain the perfect mixed venous specimen and measure cardiac output, was first performed in 1929 by the German urologist Forssmann,5 using a ureteral catheter to access his own right atrium. Over a decade later, Cournand and Richards at Columbia University in New York subsequently used right heart catheterization to record pulmonary artery pressure (PAP) in patients with shock and secondary forms of pulmonary hypertension (PHT). For these accomplishments, which were inspired by an interest in the pulmonary circulation and PHT related to mitral stenosis, Forssmann, Cournand, and Richards received the Nobel Prize in 1956. [ABSTRACT FROM AUTHOR]

Each year in the United States, an estimated 5 million people suffer an episode of venous thrombosis,1 650,000 experience a pulmonary embolic event,2 and as many as 200,000 of them die.3 Although pulmonary thromboembolism (PTE)* occurs in all age groups, most victims are middle-aged or older.4 A concurrent illness usually is present, but PTE can strike seemingly healthy, active persons,5 including children6 and adolescents.7 [ABSTRACT FROM AUTHOR]

Current nonpharmacologic treatments for cardiac arrhythmias include catheter ablation, placement of pacemakers or cardioversion/defibrillator devices, and surgery. These modalities can cure most supraventricular and ventricular tachyarrhythmias. Although the indications for surgical intervention have narrowed, surgery remains an important treatment option, especially for the most common of all arrhythmias, atrial fibrillation. [ABSTRACT FROM AUTHOR]

The implantable cardioverter-defibrillator (ICD) is designed to rapidly and accurately detect malignant ventricular arrhythmias and deliver a sufficient amount of energy to terminate the arrhythmia before there is any end-organ damage from the cardiac arrest.Although dual-chamber tachycardia detection may give a clinician more confidence in diagnosing appropriate therapy, it is unclear whether this justifies the additional risk and expense of the atrial lead insertion.Electromagnetic interference generated from electrocautery, lithotripsy, or radiofrequency ablation can create electrical signals recorded by the device as ventricular depolarizations.Implantable cardioverter-defibrillators for primary prevention of sudden death is not recommended for individuals immediately after myocardial infarction or coronary artery revascularization, although many of these patients will ultimately meet criteria for prophylactic ICD implantation as demonstrated by the MADIT-II and SCD-HeFT trials.Most ICD trials performed in the past decade clearly demonstrate mortality benefits in patients identified as high risk for sudden death. [ABSTRACT FROM AUTHOR]

Cardiac pacing is performed for treatment of patients with bradyarrhythmias and tachyarrhythmias, although for the latter category, cardiac defibrillators are more efficacious.Atrial pacing is referred to as "physiologic pacing" and its advantage is the ability to provide near-normal hemodynamics both at rest and during exercise.In the United States, the majority of pacemakers utilizing this mode are dual chamber, and the choice of programming of these devices to DDD versus DDDR mode (see Table 100.1) is determined by the presence of chronotropic incompetence.Prominent manifestations of pacemaker syndrome include orthostatic hypotension, syncope or near syncope, fatigue, exercise intolerance, lightheadedness, malaise, weakness, lethargy, dyspnea, symptoms of congestive heart failure, cough, neck pulsations or head/chest fullness-pressure, headache, chest pain, altered mentation, and effort intolerance.Displacement of an implanted lead is one of the commonest complications.Lead perforation can produce a variety of symptoms ranging from the development of cardiac tamponade or failure to thrive. Lead perforation is seen more commonly in older patients, especially women, and may be recognized when the patient develops pericardial chest pain after the implant with or without alterations in the pacing and sensing thresholds. A pericardial friction rub may be audible if a significant effusion has not developed.Electrocautery is one of the most common potential hospital sources of electromagnetic interference and is most commonly seen with unipolar devices. [ABSTRACT FROM AUTHOR]

Antiarrhythmics, like many other drugs, produce widely divergent actions in patients: the spectrum of responses range from suppression of highly symptomatic arrhythmias to inefficacy or provocation of lifethreatening arrhythmias by the drugs themselves. Elucidation of the mechanisms underlying this striking variability in drug response has been useful not only for improving therapy with available antiarrhythmic drugs, but also for pointing to new mechanisms in arrhythmias and new therapies. In addition, study of the variability in antiarrhythmic drug action has elucidated principles broadly applicable to pharmacotherapy, involving the genetics of drug responses, the role of active metabolites in drug therapy, and general principles in mechanisms of adverse drug responses. [ABSTRACT FROM AUTHOR]

Sudden cardiac death (SCD) is the unexpected natural death from cardiac cause that occurs spontaneously or within 1 hour from the onset of abrupt change in clinical status in a person without a prior condition that would have appeared to be fatal.This incidence of SCD ranges from 36 to 128 per 100,000 inhabitants per year in different studies.The epidemiology of SCD parallels that of coronary artery disease (CAD).The annual incidence of SCD is three to four times higher in men than in women.The most important predictor of SCD is a left ventricular ejection fraction (LVEF) <30%.Coronary artery disease is the most common cause of SCD in Western countries.The incidence of SCD associated with hypertrophic cardiomyopathy (HCM) is 2% to 4% per year, and it is higher in younger than older patients with HCM.Arrhythmogenic right ventricular dysplasia is a rare but important cause of SCD in young, otherwise healthy people. It should be considered in patients with frequent ventricular premature beats (VPBs) or ventricular tachycardia (VT), especially if the ventricular arrhythmias have left bundle branch block (LBBB) morphology.Symptomatic valvular aortic stenosis is one of the most common noncoronary causes of SCD.Approximately 10% of SCDs in the adult population occur in patients with dilated cardiomyopathies.Patients with long QT syndrome, short QT syndrome, and Brugada's syndrome also have increased risk of SCD.Beta-blocker therapy may reduce the risk of SCD after myocardial infarction (MI).Amiodarone has a reduced risk of SCD in several clinical trials.The implantable cardioverter defibrillator reduces the risk of SCD in patients with moderately severe left ventricular (LV) dysfunction and CAD. [ABSTRACT FROM AUTHOR]

Ninety percent of broad QRS tachycardia patients presenting to the emergency room are ventricular tachycardias (VTs).Atrioventricular dissociation in VT is characterized by irregular cannon A waves in the jugular venous pulse, varying intensity of the first heart sound, beat-to-beat changes in the systolic blood pressure.Independent beating of atria and ventricles during VT can result in "capture" or "fusion beats."Ninety percent of cases of VT have a QRS duration of more than 0.14 second and virtually all supraventricular tachycardias (SVTs) with aberrant conduction have a QRS duration of <0.14 second.Most VTs have a prior myocardial infarction as their etiology.Idiopathic VTs may have their origin in the RV or LV.When a wide QRS tachycardia is not tolerated hemodynamically, emergent cardioversion should be performed. [ABSTRACT FROM AUTHOR]

Atrial fibrillation is the most common sustained arrhythmia.For patients presenting with their first episode of atrial fibrillation, transthoracic echocardiography is often helpful for initial management and evaluation. Many cardiac disorders associated with atrial fibrillation, including mitral valve disease, hypertensive heart disease [left ventricular (LV) hypertrophy], or focal ischemic heart disease (segmented LV systolic dysfunction) may be recognized by transthoracic echocardiography.The absence of both clinical risk factors and structural heart disease in transthoracic echocardiography identifies patients for whom chronic therapy with aspirin as opposed to warfarin may be preferred. Transthoracic echocardiography is not advocated for identification or exclusion of atrial thrombi because of its inability to detail small thrombi and to image the left atrial appendage. For the detection of left atrial thrombi, transesophageal echocardiography (TEE) is superior.The author recommends cardioversion for most patients who present with their first episode of atrial fibrillation (assuming the duration of the atrial fibrillation is brief, and reversible potential causes of atrial fibrillation have been treated).Patients with persistent atrial fibrillation of more than 1 year and those with a left atrial dimension of more than 6.0 cm are less likely to have long-term maintenance of sinus rhythm.Patients with atrial fibrillation for at least 2 days have a 6% risk of cardioversion-related clinical thromboembolism if cardioversion is not preceded by 3 to 4 weeks of warfarin.Transesophageal echocardiography may be beneficial in guiding early cardioversion and detecting left atrial thrombi.Systemic anticoagulation for 4 weeks after cardioversion inhibits the formation of new thrombi during the recovery of atrial function, and can be used for prophylaxis should the patient revert to atrial fibrillation.The presence of an atrial thrombus by TEE confers an adverse prognosis despite maintenance of systemic anticoagulation and avoidance of cardioversion. [ABSTRACT FROM AUTHOR]

A common cause of chronic abnormalities in the atrioventricular (AV) conduction system is age-related fibrosis.AV nodal block in acute inferior infarction is usually caused by an occlusion of the proximal part of the right coronary artery.Block distal to the AV node (in His or the Bundle Branch System) in acute anterior infarction indicates a very proximal occlusion in the left anterior descending coronary artery.Both AV nodal and subnodal conduction abnormalities in acute myocardial infarction increase mortality. This still holds in the reperfusion era.In chronic AV block the site of block in the AV conduction system can usually be determined non-invasively.Left bundle branch block may hamper the diagnosis of myocardial infarction. The decision to give reperfusion therapy should be based upon the clinical impression.The cardiologist should be familiar with paroxysmal complete AV block.Site and mechanism of AV block should determine decision making about pacemaker implantation. [ABSTRACT FROM AUTHOR]

Wolff, Parkinson, and White described patients with electrocardiograms (ECGs) showing a short PR interval, a delta wave, and a wide QRS complex. Wolferth and Wood postulated the presence of an accessory AV pathway to explain the unusual ECG and the frequently occurring tachycardias in these patients.Ventricular preexcitation should be understood as activation of the ventricles occurring over two atrioventricular (AV) pathways, resulting in a fusion QRS complex whose configuration depends on the contribution of each of the two activation fronts.Orthodromic circus movement tachycardia (CMT) has AV conduction over the AV node and ventricularatrial conduction over the accessory AV pathway. A tachycardia moving in the reverse direction, that is, AV conduction over the accessory pathway and ventricularatrial conduction over the His-AV node, is called an antidromic one.In patients having a rapidly conducting accessory pathway, atrial fibrillation can be extremely dangerous.An accessory AV pathway with a short anterograde refractory period may lead to life-threatening high ventricular rates if atrial fibrillation supervenes.The patient with preexcitation and arrhythmias can usually have these arrhythmias cured by catheter ablation of the accessory pathway.There is controversy about how to manage the asymptomatic patient. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF) has been recognized as a distinct rhythm since the beginning of the 20th century.1 In clinical practice, AF is the most common sustained arrhythmia encountered, yet it remains one of the greatest challenges in the field of heart rhythm disorders. Based on epidemiologic data, close to 1% of persons older than 60 years suffer from AF, increasing to more than 5% of persons aged 70 years and older, with the rate of newly diagnosed AF approximately effectively doubling with each decade.2 Overall, one in four men and women after age 40 are destined to develop AF, falling only slightly to one in six in persons without prior history of cardiac disease such as myocardial infarction (MI) or congestive heart failure.3 Over the past 30 years, data from the Rochester Epidemiology Project are consistent with these findings, pointing to a significant increase in the age-adjusted prevalence of AF in patients with ischemic stroke when compared with age- and gender-matched controls and was observed both in males and females.4 In the United States this translates to roughly 2.3 million people affected by AF, a figure projected to increase to around 3.3 million by 2010 and 5.6 million by 2050.5 Added to this, the proportion of patients with AF older than 80 years is expected to exceed 50% by 2050 (Fig. 92.1). In all, AF represents a growing epidemic. [ABSTRACT FROM AUTHOR]

Supraventricular tachyarrhythmias (SVTs) are those tachycardias in which structures above the division of the bundle of His into the bundle branches are essential for their occurrence.The width of the QRS complex during SVT ranges usually from 80 to 100 ms. Supraventricular tachyarrhythmia may present with a QRS complex of 120 ms or more when (1) permanent bundle branch block is present; (2) functional bundle branch block develops because of the rate of the tachycardia; (3) atrioventricular (AV) conduction during the SVT goes over an accessory AV pathway.With atrial tachycardia, typically during the tachycardia, the electrocardiogram (ECG) shows that the P wave precedes the QRS complex, and the atrial rate during the tachycardia varies from 120 to 240 beats per minute.Atrial flutter is associated with macro reentry in the right atrium with a regular atrial rate of 250 to 350 beats per minute and a ventricular rate that depends on AV nodal transmission characteristics. In most atrial flutter patients, the cavo-tricuspid isthmus is part of the flutter circuit. This is the area where catheter ablation is able to interrupt the reentry mechanism and cure the patient.The most common type of atrial ventricular nodal reentry tachycardia (AVNRT) typically shows simultaneous activation of the atrium and the ventricle during the arrhythmia.Accelerated atrioventricular junctional rhythms may occur with myocardial ischemia, with inflammation, after cardiac surgery, and in digitalis intoxication.Accessory connections between the atrium and ventricle frequently participate in tachycardia circuits [atrioventricular reciprocating tachycardia (AVRT)].Alternating changes in the QRS complex during a narrow QRS tachycardia are highly suggestive of AVRT.Adenosine given intravenously is the drug of choice for patients with SVT unless the patient has a history of bronchospasm.Atrial flutter can best be terminated pharmacologically by ibutilide.In most supraventricular tachycardias definitive cure is possible by catheter ablation therapy. [ABSTRACT FROM AUTHOR]

Sinus node dysfunction (SND) encompasses a broad array of disturbances of sinus node or sinoatrial (SA) function that result in chronic or intermittent periods of slow or fast heart beating.Sinus node dysfunction may be the result of conditions that directly alter sinus node or SA structure, such as ischemic changes, fibrosis or infiltrative diseases, or extrinsic factors, such as drugs or autoimmune disturbances.In children and young adults, intrinsic SA disease has been most commonly associated with presumed direct sinus node damage due to previous atrial surgery, such as closure of atrial septal defects (ASDs), and most importantly, after atrial switch procedures for transposition of the great arteries. However, SND has been observed in patients with unoperated congenital heart disease and even in apparently normal children and adolescents.Thromboembolism is the single most important cause of mortality in SND. Its incidence ranges from 15% to 38%.Regarding therapy of SND, pacemaker therapy may be appropriate in some cases, drug suppression of arrhythmias in others, and both strategies may be required in many individuals.Anticoagulation is critical for treatment of many individuals with SND, particularly those with paroxysmal or persistent atrial fibrillation.In general, pacemaker therapy is indicated and has proven to be highly effective in patients with SND when bradyarrhythmia has been demonstrated to account for symptoms. [ABSTRACT FROM AUTHOR]