Search

OBJECTIVE: To measure the association between cardiac structure and function abnormalities and isolated metabolic syndrome (metabolic syndrome excluding established hypertension or diabetes mellitus). PARTICIPANTS AND METHODS: We collected data prospectively [...]

Hemorrhagic shock (HS) is associated with cardiac contractile dysfunction. Mast cell (MC) degranulation is hypothesized to mediate the cardiodepressant effect. Cardiac function was assessed after HS and resuscitation (HS/R) with the administration of the MC stabilizers to prevent MC degranulation. Anesthetized male Sprague-Dawley rats were randomized to sham-operated control or HS/R groups and underwent 60 min of HS followed by 2 h of resuscitated reperfusion. Animals in the HS/R groups were randomized to receive cromolyn (5 mg/kg), ketotifen (1 mg/kg), or saline 15 rain before shock. Hearts were excised following HS or 2 h of reperfusion, and function was assessed on a Langendorff apparatus. A second group of randomized animals had serial blood samples taken to assess MC degranulation by quantifying levels of serum [beta]-hexosaminidase. Hearts were excised at 0 min (before HS) and following 60 min of HS (before resuscitation) for a histological evaluation of MC density and degranulation. In vivo MC stabilization using ketotifen and cromolyn improved cardiac peak systolic pressure (P < 0.05), contractility (P < 0.05), and relaxation (P < 0.05) compared with that of HS controls. Serum [beta]-hexosaminidase increased during HS/R and was inhibited by MC stabilization (P < 0.05). Degranulation was inhibited when assessed by histochemistry and immune fluorescence. The inhibition of MC degranulation can significantly improve cardiac function following HS/R. [beta]-hexosaminidase; rat mast cell protease-1; left ventricular dysfunction; Langendorff apparatus: cytokines

We hypothesized that cardiac dysfunction in hypothyroidism is mainly caused by the impairment of [Ca.sup.2+] handling in excitation-contraction coupling. To prove this hypothesis, we investigated left ventricular (LV) mechanical work and energetics without interference of preload and afterload in an excised, blood-perfused whole heart preparation from hypothyroid rats. We found that LV inotropism and lusitropism were significantly depressed, and these depressions were causally related to decreased myocardial oxygen consumption for [Ca.sup.2+] handling and for basal metabolism. The oxygen costs of LV contractility for [Ca.sup.2+] and for dobutamine in the hypothyroid rats did not differ from those in age-matched normal rats. The expression of sarco(endo)plasmic reticulum [Ca.sup.2+]-ATPase (SERCA2) significantly decreased and that of phospholamban significantly increased. The present results revealed that changes in LV energetics associated with decreased mechanical work in hypothyroid rats are mainly caused by the impairment of [Ca.sup.2+] uptake via SERCA2. We conclude that the impairment of [Ca.sup.2+] uptake plays an important role in the pathogenesis of cardiac dysfunction in hypothyroidism. pressure-volume relationship; isomyosin; hypothyroidism; contractility; sarcoplasmic reticulum calcium adenosinetriphosphatase

The angiotensin-converting-enzyme (ACE) gene does not appear to significantly influence left ventricular mass or increase the genetic risk of developing an enlarged left heart heart. It has been speculated that carriers of the D allele of the ACE gene have a greater incidence for some heart disorders, especially those involving the left ventricle. DNA samples and echocardiographic data from 2,439 people were compiled and compared to identify any risk of left ventricular problems associated with the ACE gene. No difference in the prevalence of left ventricular mass or heart enlargement was found to be related to any particular genotype of the ACE gene. Further comparisons of the genotypes and polymorphic data found no relationship between the ACE locus and left ventricular mass.

Those with a disproportionately enlarged left heart ventricle appear to have a greater risk of stroke than those with normal-sized left ventricles. The relation of left ventricular mass (LVM) to body height was determined for 1,230 men and women aged 59 to 90 who were followed for eight years. The subjects suffered a total of 62 strokes and 27 transient ischemic attacks. The rate of stroke in the 25% of men with the highest LVM-to-height ratio was 18.4%. The corresponding rate for women was 12.2%. The rate for the 25% of men with the lowest LVM-to-height ratio was 5.2%, while women with the lowest LVM-to-height ratios had a rate of 2.9%. The overall increase in risk for the 25% with the highest LVM-to-height ratios compared to the 25% with the lowest LVM-to-height ratios was 2.72 after adjusting for factors such as age, blood pressure, smoking and diabetes. Enlarged LVM should be considered a risk factor for stroke., Objective.--To evaluate the association of echocardiographically determined left ventricular mass (LVM) with incidence of stroke or transient ischemic attack in an elderly cohort. Design.--Cohort study with a follow-up period of 8 years. Setting.--Population-based sample. Subjects.--Elderly original cohort subjects of the Framingham Heart Study who were free of cerebrovascular disease and atrial fibrillation at the 16th biennial examination and who had adequate echocardiograms. This group consisted of 447 men (mean age, 67.8 years; range, 60 to 90 years) and 783 women (mean age, 69.2 years; range 59 to 90 years). Main Outcome Measures.--Age-adjusted 8-year incidence of stroke was examined as a function of baseline quartiles of LVM-to-height ratio. Proportional hazards regression was used in multivariate analyses to assess risk of stroke as a function of LVM-to-height ratio quartile, adjusting for age, sex, systolic blood pressure, hypertension treatment, diabetes, cigarette smoking, and blood lipid levels. Results.--Among the 1230 subjects eligible, 89 cerebrovascular disease events (62 strokes and 27 transient ischemic attacks) occurred during follow-up. In men, 8-year age-adjusted incidence of cerebrovascular events was 18.4% in the highest quartile of LVM-to-height ratio and 5.2% in the lowest quartile. Corresponding values in women were 12.2% and 2.9%. The hazard ratio for cerebrovascular events comparing highest to lowest quartile of LVM-to-height ratio was 2.72 (95% confidence interval [CI], 1.39 to 5.36) after adjusting for age, sex, systolic blood pressure, hypertension treatment, diabetes, cigarette smoking, and the ratio of total cholesterol to high-density lipoprotein cholesterol. After adjusting for age, sex, and cardiovascular disease risk factors, the hazard ratio for cerebrovascular events was 1.45 (95% CI, 1.17 to 1.80) for each quartile increment of LVM-to-height ratio. Conclusions.--Echocardiographically determined LVM-to-height ratio offers prognostic information beyond that provided by traditional cerebrovascular disease risk factors. Echocardiography provides information that facilitates identification of individuals at high risk for stroke and transient ischemic attack. (JAMA. 1994;272:33-36)

The six-minute walk test may be an effective and safe method for evaluation of patients with left ventricular dysfunction. Left ventricular dysfunction is caused by different types of heart disease including congestive heart failure. Among 833 patients who participated in a six-minute walk test, 6% died and 30% were admitted to the hospital over an average follow-up period of approximately eight months. Nine percent were hospitalized for congestive heart failure. Patients with the poorest performance on the test had a significantly higher risk of dying than those with the best performance. They also had a higher risk of being hospitalized for congestive heart failure. Performance on the test is ranked by the distance walked during the six-minute testing period. The six-minute walk test is inexpensive and simple to perform.

Hypertensive heart disease, or heart disease caused by hypertension, is the result of increased arterial pressure and increased resistance of peripheral blood vessels. An increased workload on the heart can cause left ventricular hypertrophy, or enlargement of the left ventricle of the heart, and cardiac disorders such as congestive heart failure, irregular heart beat and ischemic heart disease. Older individuals and those with blood pressure over 160/95 have a higher risk of developing left ventricular hypertrophy than others. Left ventricular hypertrophy is caused by an increase in heart cell size and structural changes. Activation of genes that regulate cell division also occurs. Echocardiography is the most accurate method for diagnosing patients with left ventricular hypertrophy. Patients with left ventricular hypertrophy are treated with antihypertensive drugs.

Long-term treatment with captopril may prevent cardiovascular events and increase survival in heart attack patients with asymptomatic left ventricular dysfunction. In patients with left ventricular dysfunction, the heart is not capable of pumping enough blood to the body. Of 2,231 heart attack patients with asymptomatic left ventricular dysfunction, 1,115 were treated with captopril and 1,116 received a placebo, an inactive substance, over an average of 42 months. Twenty percent of the patients treated with captopril died, compared with 25% of those who received a placebo. Eighty-four percent of the patients died from a cardiovascular cause. Treatment with captopril decreased the risk of death from all causes by 19%, and the risk of death from cardiovascular causes by 21%. Patients who have survived a heart attack have a higher risk of a heart attack or another cardiovascular event, compared to other individuals.

Congestive heart failure affects almost two million people annually; 15 to 50 percent of these patients die within one year, depending on their severity of illness. A number of drugs have been investigated for use in treating this disease. Angiotensin-converting-enzyme inhibitors, which block enzymes that are involved in the production of angiotensin, have shown promise in the treatment of congestive heart failure. (Angiotensin causes vasoconstriction, or narrowing of blood vessels.) It is thought that angiotensin-converting-enzyme inhibitors may relieve some of the symptoms of congestive heart failure and reduce the number of hospitalizations and deaths resulting from it. This study examined the effectiveness of enalapril, an angiotensin-converting-enzyme inhibitor, in treating this disease and reducing mortality. A total of 2,569 patients with congestive heart failure and decreased left ventricular ejection fraction (diminished percentage of blood pumped from the heart at the end of each heartbeat) were assessed; 1,285 patients received enalapril at various dosages, and 1,284 were given a placebo. Hospitalizations, deaths, and side effects of the drug were monitored for up to 55 months. After 48 months, 510 patients in the placebo group had died; 461 deaths were attributed to cardiovascular causes. During the same period, there were 452 deaths in the enalapril group, of which 399 were due to cardiovascular problems. The greatest reduction in mortality in the enalapril-treated patients occurred during in the first 24 months of therapy. Hospitalizations for heart failure were required for 736 patients in the placebo group and 613 patients who were given enalapril. Enalapril had the greatest effect in reducing hospitalization during the first year of treatment. Subgroups of patients were also assessed to determine in which patients enalapril had the most favorable effects. Results showed that enalapril was equally effective among the subgroups. Only minor side effects, including dizziness and cough, were associated with the drug. These results indicate that enalapril can significantly reduce mortality and the need for hospitalization in patients suffering from congestive heart failure. (Consumer Summary produced by Reliance Medical Information, Inc.)

The mitral valve is a heart valve that allows blood to flow from the left atrium to the left ventricle, from which it is pumped throughout the body. Theoretically, if the two leaflets of the mitral valve are left in place during mitral valve repair or replacement, postoperative left ventricular (LV) function should be improved. The records of seven patients who underwent mitral valve replacement with the leaflets preserved were reviewed. All the patients were at higher than average risk. All were over 60 years old, had evidence of congestive heart failure, and underwent concurrent coronary artery bypass or other heart surgery. Left ventricular functioning did not improve after surgery, and worsened in two of the patients. Ultrasound imaging indicated that six of the patients showed evidence of LV outflow tract obstruction. The possible causes of the obstruction are discussed. Adverse clinical outcomes included 100 percent mortality. Although these patients were initially at high risk, outcomes were probably aggravated by LV outflow obstruction after mitral valve replacement with the leaflets retained. It is concluded that preservation of the anterior (front) leaflet during mitral valve replacement may adversely affect patient outcome. (Consumer Summary produced by Reliance Medical Information, Inc.)

Coronary artery bypass graft (CABG) surgery, in which a heart artery is replaced with another blood vessel, usually from the leg, is often used after a heart attack to restore blood flow (reperfusion) to damaged areas of the heart. The results of bypass surgery have been promising, but intravenous thrombolytic (clot-dissolving) therapy has also been successful in improving heart muscle function and in reducing mortality. Among the 25 percent of patients for whom clot-dissolving drugs fail, bypass surgery or angioplasty (opening of an artery using a catheter threaded up through the groin) may reduce mortality, even when the improvements are not measurable. Three hundred and three heart attack patients underwent coronary bypass surgery after treatment with drugs to reopen blocked arteries. These patients tended to be older and sicker than the patients who did not undergo surgery, but mortality did not differ significantly between the two groups. The patients who underwent CABG had greater functional recovery, determined by the function of the region of the heart damaged by the heart attack, and as measured by left ventricular ejection fraction (the proportion of blood ejected by contraction of the ventricle, relative to the total amount of blood in the ventricle). The results suggest that CABG may improve left ventricular function, as well as mortality, when it is used as part of the treatment strategy to reopen blocked arteries for heart attack patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

The left anterior descending artery supplies blood to two thirds of the left ventricular heart muscle. Acute myocardial infarction (AMI), or heart attack, in this area is especially deadly. Aggressive treatment with emergency percutaneous transluminal coronary angioplasty (PTCA), a threaded catheter is place in the artery, where the balloon tip is inflated to compress the blockage, has been encouraged. Circulation through the damaged vessel and left ventricular function are indicators of early and late survival. PTCA restores the circulation in 90 percent of blocked vessels, but 10 percent will become blocked again (reoccluded). Low blood pressure (hypotension) often occurs before reocclusion, so maintaining arterial pressure may help prevent subsequent blockage. The intraaortic balloon pump (IABP), attached to a catheter, is threaded up into the aorta, the main artery leaving the heart, where it lowers systolic (contracting) pressure and increases diastolic (resting) pressure. This decreases the work of the heart and increases the flow of blood to the coronary arteries. After sustaining a heart attack treated by emergency PTCA, 48 patients underwent IABP, and the results were compared with 66 similar patients who were not treated with IABP. The reocclusion rate was under 3 percent in the group receiving IABP, but was almost 18 percent in the group not treated with IABP. The group with IABP also showed improved left ventricular function, which was twice that of the untreated group. Vascular complications from IABP occurred in two patients, but no deaths were attributable to the procedure. (Consumer Summary produced by Reliance Medical Information, Inc.)

People who are obese are at greater risk of coronary heart disease, congestive heart failure, stroke, and death from other cardiovascular causes. They are also more likely to suffer from hypertension, glucose intolerance (associated with diabetes), lower levels of high-density lipoproteins (the 'good' cholesterol), and a type of cardiomyopathy (disease of the heart muscle). It also appears that obesity is related to left ventricular hypertrophy, or enlargement of the left ventricle of the heart. (The left ventricle pumps freshly oxygenated blood to the body.) Studies of extremely obese people have found increases in left ventricular mass, wall thickness, and cavity size. No studies have evaluated these factors in mild to moderately obese persons and compared the results with similar findings in subjects with normal weight. Echocardiography, which relies on ultrasound, now provides a noninvasive method of imaging the heart and evaluating left ventricular mass. Images of the hearts of 3,922 participants in the Framingham Heart Study were obtained to study the relation between left ventricular mass and obesity in apparently healthy people who did not have high blood pressure. It was found that even mild to moderate obesity was associated with increases in left ventricular wall thickness and internal dimension in both men and women. These changes may increase the risk of heart disease in obese people. It is known that left ventricular hypertrophy is associated with an increase in cardiovascular illness and death, and previous research has shown a greater risk of congestive heart failure among obese subjects. (Consumer Summary produced by Reliance Medical Information, Inc.)

Acute myocardial infarction (AMI; heart attack) occurs when there is an acute blockage of one or more of the coronary arteries supplying blood to the heart. The resulting reduction of cardiac blood flow (myocardial ischemia) can cause permanent damage to the heart, or death, if not reversed promptly. One complication that can result from AMI is the formation of a thrombus, or blood clot, in the heart that can migrate to the cerebral vasculature, where blockade of the cerebral circulation can have disastrous consequences in the form of a stroke. To determine the effect of combined thrombolytic (clot-dissolving) therapy using recombinant tissue-type plasminogen activator and anticoagulant therapy using heparin and aspirin, a study was carried out involving 153 AMI patients. All patients were under the age of 72, had severe chest pain for between 30 minutes and 4 hours prior to therapy, had electrocardiographically diagnosed AMI, and no additional complicating factors. Patients were treated as soon as possible after symptom onset with the three-drug combination. Of the 76 patients with anterior wall AMI (in which the blood supply to the anterior portion of the heart was occluded), seven (9.2 percent) developed thrombi. In the remaining 68 patients with inferior wall AMI (affecting the lower portion of the heart), two (2.9 percent) developed thrombi. During a 12-month follow-up period, no patients had any evidence of peripheral thrombus. Since anterior wall AMI is usually associated with thrombus formation in between 25 and 40 percent of patients, the low incidence of this complication in the current study suggests that the combined thrombolytic and anticoagulant therapy was effective. (Consumer Summary produced by Reliance Medical Information, Inc.)