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Aortic remodeling after dissection is poorly understood and remains a focus of current research. In the present report, we have described the cases of two patients with acute lower extremity ischemia related to malperfusion from aortic dissection treated with extra-anatomic axillobifemoral bypass. During long-term follow-up, aortic remodeling led to reinstitution of flow through the native aorta. This resulted in competitive flow, leading to complete thrombosis of the extra-anatomic conduits. These cases highlight the occurrence of spontaneous aortic recanalization and subsequent competitive flow, two vascular phenomena that are not well understood but can significantly affect patient outcomes.

By July 2021, the United States had over 34.4 million confirmed COVID-19 cases. Various cardiovascular manifestations of COVID-19 have been reported including ST-elevation myocardial infarction (STEMI), and there is concern that SARS-CoV-2 may be associated with a higher thrombus burden. We performed a retrospective chart review of 535 adult patients with COVID-19 admitted at Yale-New Haven Health Greenwich Hospital from February 1, 2020, to May 13, 2020. All admitted patients had undergone testing for serum troponin I and various inflammatory markers, and we identified three patients who were diagnosed with acute STEMI. Data was collected via manual chart review and included patient demographics, comorbidities, laboratory tests, electrocardiogram (ECG) results, echocardiography results, diagnoses during hospitalization, inpatient therapies, and outcomes including length of hospital stay, revascularization results, and mortality. Three of our patients had obstructive coronary artery disease confirmed via angiography. One subject was noted to display vasospasm in addition to coronary atherosclerotic obstruction and refractory thrombus formation. Among our patients with COVID-19 and STEMI, presentations were variable in terms of timing of onset of ECG changes, age, gender, race, comorbidities, symptomology, and outcomes.

Background Tako-tsubo stress cardiomyopathy is a clinical syndrome marked by transient reduction of left ventricular function in the setting of emotional or physical stress and in the absence of obstructive coronary artery disease. We describe a case of an atypical variant of Tako-tsubo in a male patient following an elective direct current cardioversion (DCCV). Case summary A 78-year-old male whose atrial fibrillation persisted after earlier unsuccessful direct current DCCV and radiofrequency ablations presented to the emergency department for acutely worsening dyspnoea and orthopnoea 12 h following his most recent DCCV. Previously, he was known to have non-obstructive coronary artery disease. Evaluation was notable for troponin I 0.019 ng/mL (negative Discussion Only five other cases of cardioversion mediated Tako-tsubo cardiomyopathy have been reported in the literature. To our knowledge, this is the first case of DCCV-induced atypical Tako-tsubo cardiomyopathy. Although overall prognosis is favourable, some have been observed to require advanced support therapy. Given risk for life-threatening complications, patients undergoing cardioversion should be educated on symptoms of congestive cardiomyopathy.

Percutaneous carotid artery stenting (CAS) has emerged as a less invasive alternative to carotid endarterectomy for the treatment of carotid atherosclerotic disease. The main risk of CAS is the occurrence of neuro-vascular complications; however, carotid artery stenting-related dysautonomia (CAS-D) (hypertension, hypotension, and bradycardia) is the most frequently reported problem occurring in the periprocedural period. Alterations in autonomic homeostasis result from baroreceptor stimulation, which occurs particularly at the time of balloon inflation in the region of the carotid sinus. The response can be profound enough to induce asystole or even complete cessation of postganglionic sympathetic nerve activity. Frequency and factors predisposing a patient to CAS-D have been investigated in several studies; however, there are significant discrepancies in results among reports. Lack of consistent findings may arise from using different methods and definitions, as well as other factors discussed in detail in this review. Furthermore, a correlation of CAS-D with short and long-term outcomes has been investigated only in small and mostly retrospective studies, explaining why its prognostic significance remains uncertain. In this manuscript, we have focused on risk factors, pathophysiology and management of periprocedural autonomic dysfunction. As there is no standardized approach to the treatment of CAS-D, we present an algorithm for the periprocedural management of patients undergoing CAS. The proposed algorithm was developed based on our procedural experience as well as data from the available literature. The Yale Algorithm was successfully implemented at our institution and we are currently collecting data for short- and long-term safety. © 2014 Wiley Periodicals, Inc.

Acute coronary syndromes and acute myocardial infarctions are often related to plaque rupture and the formation of thrombi at the site of the rupture. We examined fresh coronary thrombectomy specimens from patients with acute coronary syndromes and assessed their structure and cellularity. The thrombectomy specimens consisted of platelets, erythrocytes and inflammatory cells. Several specimens contained multiple cholesterol crystals. Culture of thrombectomy specimens yielded cells growing in various patterns depending on the culture medium used. Culture in serum-free stem cell enrichment medium yielded cells with features of endothelial progenitor cells which survived in culture for a year. Immunohistochemical analysis of the thrombi revealed cells positive for CD34, cells positive for CD15 and cells positive for desmin in situ, whereas cultured cell from thrombi was desmin positive but pancytokeratin negative. Cells cultured in endothelial cell medium were von Willebrand factor positive. The content of coronary thrombectomy specimens is heterogeneous and consists of blood cells but also possibly cells from the vascular wall and cholesterol crystals. The culture of cells contained in the specimens yielded multiplying cells, some of which demonstrated features of haematopoietic progenitor cells and which differentiated into various cell-types.

Renal artery stenting may improve blood pressure (BP) and renal function in resistant hypertension patients; however, benefit may differ depending on the degree of renal dysfunction. The authors analyzed 67 consecutive patients receiving stenting for obstructive renal artery disease between 2002 and 2005. Patients were categorized as normal or mildly impaired according to estimated glomerular filtration rate (eGFR) (or =60 mL/min/1.73 m(2)), moderately impaired (eGFR 30 to 59 mL/min/1.73 m(2)), and severely impaired (eGFR30 mL/min/1.73 m(2)). In patients with eGFRor =60, systolic BP did not significantly improve from baseline. However, in patients with an eGFR between 30 and 59 mL/min/1.73 m(2), systolic BP decreased by 12 mm Hg at 6 months (P=.02) and 14 mm Hg at 12 months (P=.01). Greater benefit was observed in patients with eGFR30 mL/min/1.73 m(2), with a 16 mm Hg (P=.10) and 21 mm Hg (P=.02) decrease at 6 and 12 months, respectively. Renal function was stable across all groups. Renal artery stenting reduced BP and produced greatest benefit in patients with baseline impaired renal function.

Distal embolic protection (DEP) may prevent embolization of atherosclerotic debris during renal artery stenting. The authors retrospectively identified 48 hypertensive patients with chronic kidney disease (CKD) who underwent renal artery stenting between 2002 and 2005 and compared stenting alone (n=17) to stenting/DEP (n=31). Blood pressure (BP) and estimated glomerular filtration rate (eGFR) (mL/min/1.73m(2)) at baseline at 6 and 12 months were compared. Overall, eGFR improved by 4.7 (P=.005) at 6 months and 3.8 (P=.003) at 12 months compared with baseline. Comparing stent to stent/DEP patients, eGFR improvement did not differ at 6 months (7.6 vs 2.9; P=.15) or at 12 months (4.4 vs 3.5; P=.74). Systolic BP reduction was similar between stent and stent/DEP patients at 6 months (−9 vs −14 mm Hg; P=.59) and at 12 months (−18 vs −16 mm Hg; P=.89). Renal artery stenting improved eGFR and systolic BP in patients with hypertension and CKD; however, DEP did not enhance these effects.

The epidemic of obesity in the United States and around the world is intensifying in severity and scope and has been implicated as an underlying mechanism in systemic hypertension. Obese hypertensive individuals characteristically exhibit volume congestion, relative elevation in heart rate, and high cardiac output with concomitant activation of the renin-angiotensin-aldosterone system. When the metabolic syndrome is present, insulin resistance and hyperinsulinemia may contribute to hypertension through diverse mechanisms. Blood pressure can be lowered when weight control measures are successful, using, for example, caloric restriction, aerobic exercise, weight loss drugs, or bariatric surgery. A major clinical challenge resides in converting short-term weight reduction into a sustained benefit. Pharmacotherapy for the obese hypertensive patient may require multiple agents, with an optimal regimen consisting of inhibitors of the renin-angiotensin-aldosterone system, thiazide diuretics, beta-blockers, and calcium channel blockers if needed to attain contemporary blood pressure treatment goals.

Background: Myocardial infarction in pregnancy carries high morbidity. Spontaneous coronary artery dissection is one etiology of infarction, and up to one third of cases may arise in the third trimester of pregnancy or within three months postpartum.Case: We report two cases of spontaneous coronary artery dissection, one at 34 weeks gestation and one postpartum. Both patients were diagnosed with angiography and treated medically and one required percutaneous coronary intervention, with good obstetric outcome and return of cardiac function.Conclusion: Myocardial infarction, and particularly spontaneous coronary artery dissection, should be in the differential diagnosis of pregnant women presenting with cardiac-type symptoms, despite perceived lack of risk factors. Angiography will aid in diagnosis, and multiple therapeutic modalities exist.

Ischemic heart disease (IHD) affects about 16 million adults in the USA. Many more individuals likely harbor subclinical coronary disease. Hypertension (HTN) continues to be a potent and widespread risk factor for IHD. Among other Framingham risk factors of tobacco use, diabetes mellitus, dyslipidemia, and left ventricular hypertrophy, HTN plays an independent role in augmenting IHD risk, as well as a multiplicative role with respect to adverse outcomes when HTN is present concurrently with the other major IHD risk factors listed above. Over the past two decades, numerous studies and guideline reports have been presented with the aims of (a) elucidating the pathophysiology of IHD, (b) delineating an ideal blood pressure (BP) threshold at which to institute pharmacotherapy, and (c) defining the optimal pharmacologic elements of a therapeutic regimen. While there are active debates surrounding the existence and relevance of the J curve in IHD patients who have HTN, as well as the numerical level of the BP cutoff justifying drug therapy in the general population, there is a general consensus that the BP target in IHD patients should be lower than 140/90 mmHg. The most appropriate class (or classes) of medication recommended will depend on the comorbid conditions associated with each individual patient. Overall, however, there is no major evidence underscoring a significant difference between drug classes, provided the target BP is achieved, although it should be pointed out that the most recent (2015) American Heart Association (AHA)/American College of Cardiology (ACC)/American Society of Hypertension (ASH) guideline statement now elevates beta-blockers (BB) to the same level of recommendation as other classes of hypertension drugs in the treatment of patients who have hypertension and ischemic heart disease. Although most agents that reduce blood pressure will correspondingly lower myocardial workload, BB may exhibit a special advantage in IHD patients because BB (as well as verapamil and diltiazem subclasses of calcium channel blockers or CCB) act to lower HR as well as cardiac inotropy. Moreover, BB will remain an integral if not indispensable part of the management of IHD, especially in those with history of angina pectoris or MI, based on decades of favorable clinical as well as trial experience. This extensive salutary historical background has served as a foundation for the 2015 committee's decision to bring BB into the front rank of BP agents for those hypertensive individuals suffering simultaneously from IHD.

A 70-year-old woman with a long-standing history of hypertension comes for follow-up. Her medications include atenolol (100 mg daily), hydrochlorothiazide (12.5 mg daily), lisinopril (40 mg daily), and ibuprofen (400 mg twice daily for osteoarthritis). She does not smoke or drink alcohol. Her body-mass index (the weight in kilograms divided by the square of the height in meters) is 32. Her systolic and diastolic blood pressures (measured three times while she was seated) range from 164 to 170 mm Hg and 92 to 96 mm Hg, respectively, and the pulse rate is 72 per minute. Examination of her ocular fundi reveals arteriolar narrowing. The results of cardiovascular examination are normal. There are no abdominal bruits. The serum potassium level is 3.8 meq per liter, and the serum creatinine level is 1.2 mg per deciliter (106 μmol per liter); there is no microalbuminuria. How should this patient be further evaluated and treated?

Although asymptomatic pericardial effusions are relatively common in pregnancy, their true incidence is not known. Symptomatic effusions are, however, rare in pregnancy. The authors present a rare case of pericardial tamponade complicating pregnancy with resulting diagnosis of angiosarcoma. They review the literature involving pericardial disease in pregnancy and discuss important issues in management and include a discussion of angiosarcoma.

OBJECTIVE—Thiazolidinediones (TZDs) and metformin are insulin-sensitizing antihyperglycemic agents with reported benefits on atherosclerosis. Despite extensive use in patients with diabetes and cardiovascular disease, there is a paucity of outcomes data with metformin and none yet with TZDs. We sought to determine the impact of these insulin sensitizers on outcomes in diabetic patients after hospitalization with acute myocardial infarction (AMI).RESEARCH DESIGN AND METHODS—We conducted a retrospective cohort study of 24,953 Medicare beneficiaries with diabetes discharged after hospitalization with AMI between April 1998 and March 1999 or July 2000 and June 2001. The independent association between discharge prescription for metformin, TZD, or both agents and outcomes at 1 year was assessed in multivariable Cox proportional hazards models, adjusting for patient, physician, and hospital variables. The primary outcome was time to death within 1 year of discharge; secondary outcomes were time to first rehospitalization within 1 year of discharge for AMI, heart failure, and all causes.RESULTS—There were 8,872 patients discharged on an antihyperglycemic agent, of which 819 were prescribed a TZD, 1,273 metformin, and 139 both drugs. After multivariable analysis, compared with patients prescribed an antihyperglycemic regimen that included no insulin sensitizer, mortality rates were not significantly different in patients treated with either metformin (hazard ratio [HR] 0.92 [95% CI 0.81–1.06]) or a TZD (0.92 [0.80–1.05]) but were lower in those prescribed both drugs (0.52 [0.34–0.82]). The results were similar among patients with heart failure. The prescription of a TZD was associated with a borderline higher risk of all-cause readmission (1.09[1.00–1.20]), predominately due to a higher risk for heart failure readmission (1.17 [1.05–1.30]).CONCLUSIONS—Individually, prescription of insulin-sensitizing drugs is not associated with a significantly different risk of death in older diabetic patients within 1 year following AMI compared with other antihyperglycemic agents. Combined, however, metformin and TZDs may exert benefit. TZD prescription is associated with a higher risk of readmission for heart failure after myocardial infarction.

Pheochromocytomas classically present with paroxysms of hypertension and adrenergic symptoms including headaches, palpitations, tremor, and anxiety. However, these tumors can be clinically silent and occasionally present only when catecholamine release is up-regulated by exogenous stimuli. In addition, the clinical presentation of pheochromocytoma can mimic a number of more common medical conditions, including migraine headaches, cardiac arrhythmias, and myocardial infarction, making diagnosis difficult. In this report, we present the case of a young woman who, while receiving oral corticosteroid therapy for presumed migraine headaches, suffered a myocardial infarction and ultimately hemorrhaged into a previously undiagnosed pheochromocytoma. Our patient exhibited severe, labile hypertension after the administration of iv beta-blockade for presumed myocardial ischemia, raising our initial clinical suspicion for pheochromocytoma. In this paper we review some of the key clinical issues related to this complex case, including steroid-induced stimulation of catecholamine synthesis and release, the role of pheochromocytoma in myocardial ischemia and electrocardiographic changes, and the rare complication of tumor hemorrhage. We then briefly review the essential diagnostic and management strategies for this rare but potentially lethal tumor, with specific emphasis on pheochromocytoma-related cardiovascular emergencies and the surgical management of tumor hemorrhage.

This study evaluates transcoronary changes in neutrophil and platelet activation and conjugate formation in patients with angina pectoris secondary to coronary artery disease. We examined parameters of neutrophil and platelet activation as well as the neutrophil-platelet conjugate formation in patients who underwent diagnostic coronary angiography. Thirty-nine patients with chest pain referred for cardiac catheterization were studied (23 patients with unstable angina pectoris [UAP] and 16 with stable angina pectoris [SAP]). Before coronary angiography, blood samples were obtained simultaneously from the aortic root and coronary sinus to assess leukocyte (CD11b) and platelet (CD62P) activation and leukocyte-platelet conjugates. There was a 94% increase in CD62-expressing platelets from the aorta to the coronary sinus in patients with UAP compared with a 49% increase in patients with SAP. The percentage of neutrophil-platelet conjugates increased by 22% in patients with UAP compared with a 16% decrease in those with SAP (p

The use of thiazide diuretics as one of the preferred antihypertensive medications has stood the test of time. Since the introduction of orally effective agents in 1957 to 1958, these drugs have continued to prove their usefulness. Numerous clinical trials have confirmed that these medications are as or more effective in reducing blood pressure and cardiovascular events than any of the other effective antihypertensive agents. Although some metabolic changes may occur with higher dosages of these medications, they seem to be of limited clinical significance. In addition to being well tolerated and effective. thiazide-type diuretics are less expensive than other agents. This should be considered in view of the fact that quality of care is not compromised when the less expensive medication is used. beta-Blockers should also be considered as a major drug class in the management of hypertensive patients. There are few studies directly comparing these drugs with other agents. Although some data suggest that they are less effective in reducing CHD events in the elderly, there are numerous situations where beta-blockers are clearly indicated. Combination therapy with a beta-blocker and diuretic has been shown to be highly effective in reducing cardiovascular events in both diabetic and nondiabetic patients.

A 39-year-old woman with cervical cancer treated with pelvic radiation therapy and 5-fluo rouracil (5-FU) was hospitalized for dehydration and intractable vomiting. She developed an acute ST-elevation myocardial infarction (MI) that extended electrocardiographically after thrombolytic therapy. Coronary angiography demonstrated a completely occluded left anterior descending (LAD) artery with extensive coronary dissection that was treated successfully with stenting. The authors discuss several factors that may have contributed to the sponta neous coronary artery dissection (SCAD) including chemotherapy-induced vasospasm, hemo dynamic stress of vomiting, and hormonal changes associated with pelvic radiation.

The renin-angiotensin-aldosterone system (RAAS) plays an integral role in maintaining vascular tone, optimal salt and water homeostasis, and cardiac function in humans. However, it has been recognized in recent years that pathologic consequences may also result from overactivity of the RAAS. Clinical disease states such as renal artery stenosis, hypertension, diabetic and nondiabetic nephropathies, left ventricular hypertrophy, coronary atherosclerosis, myocardial infarction, and congestive heart failure (CHF) are examples. Part of the adverse cardiorenal effects of the RAAS may be related to the prominent role that this system plays in the activation of the sympathetic nervous system, the dysregulation of endothelial function and progression of atherosclerosis, as well as inhibition of the fibrinolytic system. Also, direct profibrotic actions of angiotensin II and aldosterone in the kidney and heart promote end organ injury. Current basic science and clinical research supports the use of inhibitors of the RAAS, including angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone antagonists in treating hypertension, improving diabetic nephropathy and other forms of chronic kidney disease, preventing or ameliorating CHF, and optimizing prognosis after myocardial infarction.

Aortic coarctation, a congenital narrowing in the region of the ligamentum arteriosium, is a rare etiology for multi-drug-resistant hypertension in adulthood; however, advances in stenting modalities may offer long-term improvements in morbidity and possibly even cure. We report on a female patient in her late 50s presenting with refractory hypertension and severely elevated renin levels, ultimately diagnosed with aortic coarctation and treated with percutaneous stent implantation, which resulted in successful blood pressure control with verapamil monotherapy. This case highlights the efficacy of endovascular stent implantation for the treatment of coarctation and the need for clinicians to consider this disease entity in the differential diagnosis of refractory hypertension even in late adulthood.

Although activation of the complement system in myocardial infarction and cardiopulmonary bypass has been shown to contribute to myocardial injury, its role in congestive heart failure (CHF) is unknown. The purpose of this study was to determine the presence of terminal complement activation and its relation to clinical outcomes in patients with CHF.We measured serum levels of the terminal complement complex C5b-9 in 36 patients with symptomatic heart failure and left ventricular ejection fraction40%. We compared the serum C5b-9 levels of these patients with CHF with a group of 12 age-matched control patients. Combined clinical outcomes (death, urgent heart transplantation, or hospitalization with worsening heart failure) at 6 months were determined.The serum C5b-9 [median (25th to 75th percentiles)] levels in 36 patients with CHF [101.5 ng/mL (40 to 164)] were significantly (P =.003) higher than in the 12 control patients [36.5 ng/mL (22 to 50)]. Significantly more of the patients with CHF with the highest levels of C5b-9 (highest 50th percentile) had New York Heart Association class IV symptoms (67% vs 33%; P =.04) and adverse clinical outcomes by 6 months (56% vs 17%; P =.02) compared with the patients with CHF with lower levels (lowest 50th percentile).We have described a significant elevation in circulating C5b-9, the terminal complement complex, in patients with symptomatic heart failure and have observed an association between high levels of C5b-9 and near-term adverse events.

Cocaine abuse and HIV disease each have potentially adverse effects upon the heart and cardiovascular system which may be exacerbated when these risk factors are combined. The development of a safe and effective agent to treat both cocaine addiction and its cardiovascular sequelae, that is well-tolerated by HIV patients, would thus be of considerable clinical utility. In this article we discuss the rationale for the investigation of angiotensin converting enzyme (ACE) inhibitors, commonly used to treat hypertension, for treatment in cocaine-abusing populations, based on their potential to reduce cocaine use by modulating levels of dopamine and corticotropin releasing factor in the brain, and on their ability to reverse cardiovascular and platelet abnormalities. We present preliminary findings from echocardiographic and platelet activation studies in 16 HIV-positive, cocaine abusing patients, as well as tolerability and efficacy studies of the ACE-inhibitor, fosinopril, for the treatment of cocaine abuse in both HIV-positive (n=6) and HIV-negative (n=5) methadone-maintained cocaine abusers. Findings suggest that HIV-positive cocaine-abusing patients possess abnormalities of diastolic heart function and platelet activation that are potentially reversible with ACE-inhibitor therapy. Findings also suggest that fosinopril is well-tolerated regardless of HIV serostatus, does not appear to cause hypotension, and may possess effectiveness for reducing cocaine use. We conclude that ACE-inhibitor therapy may offer a new pharmacologic approach to the treatment of cocaine abuse and its complications, and that controlled research of this class of agents may be promising.

Purpose: Captopril renal scintigraphy (CRS) is a nuclear medicine technique for evaluating each kidney independently for changes in glomerular filtration rate and perfusion induced by captopril-associated alterations in vascular tone. This study was undertaken to determine the role of CRS in predicting the response to renal revascularization. Methods: The study group consisted of all patients who underwent preintervention CRS and arteriography, followed by renal revascularization performed between December 1987 and February 1992. After cessation of administration of angiotensin-converting enzyme inhibitors for 48 hours, a standard renogram was obtained, a 50 mg dose of captopril was given, and a second renogram was obtained. A captopril-induced change in the renogram was present when a normal pre-captopril renogram became abnormal after captopril administration. An abnormal baseline scan by definition cannot have a captopril-induced change. Blood pressure before revascularization was compared with blood pressure at 3 to 6 months after the procedure according to American Heart Association criteria for hypertension response. Results: Fifty patients received renal revascularization by operation (28 patients) or balloon angioplasty (22 patients). Preoperative captopril-induced changes were present in 29 of the 50 patients. Among the 29 patients with captopril-induced changes, hypertension was cured or improved in 26. When captopril-induced changes were not present, only one of 21 patients improved ( p Conclusion: On the basis of these data, CRS appears to reliably predict hypertension response to revascularization in patients with renovascular disease. (J VASC SURG 1993;17:280-7.)

Congestive heart failure (CHF) is typically associated with impaired left ventricular (LV) systolic performance. Few reports exist describing the long-term outcome in patients with CHF and normal LV systolic function. Fifty-two patients initially hospitalized with CHF and intact LV function (ejection fraction greater than or equal to 45%) were followed for 7 years. Mean age when initially identified was 71 +/- 11 years (range 36 to 96), and average LV ejection fraction was 61 +/- 11%. CHF was graded by a clinicoradiographic index, with a mean of 7.0 +/- 2.3 (range 3 to 12, 13 indicates worst CHF). A third heart sound was present in 19 patients (37%), and 17 (33%) had presented with acute pulmonary edema. Principal cardiovascular diagnoses were coronary artery disease in 27 (52%), hypertensive heart disease in 16 (31%) and restrictive cardiomyopathy in 7 (13%). At 7 years, cardiovascular mortality was 46% (24 of 52), and noncardiovascular mortality was 10% (5 of 52). Survival was not correlated with age, principal diagnosis, third heart sound, pulmonary edema at presentation, LV ejection fraction, or presence or degree of LV diastolic dysfunction. Cardiovascular morbidity, consisting of nonfatal recurrent CHF, myocardial infarction, unstable angina or other cardiovascular events occurred in 29% (15 of 52). Combined cardiovascular mortality and morbidity was 75% (39 of 52). In patients with CHF, intact LV systolic function does not confer the same favorable prognosis it defines in other clinical situations. For such patients, the risk of future cardiovascular events is high, a finding that should be considered when designing therapeutic strategies in this group.

The right ventricle is often affected by pulmonary hypertension caused by elevated pulmonary venous pressures of left ventricular, left atrial, or pulmonary venous origin. Biochemical factors, the pericardium, the interventricular septum, and the pulmonary arterial system influence the right ventricle in these disease states. The right ventricle experiences structural and hemodynamic adaptations that permit compensation with chronic pressure overload. In uncorrected disease, late findings suggest frank right ventricular failure. Therapy to improve the primary left heart disorder permits a degree of right ventricular recovery. In cases of left heart failure, right ventricular performance may provide significant prognostic information.

Right ventricular myocardial infarction, long unrecognized because of a lack of diagnostic methods and unsupported beliefs regarding the dispensability of the right ventricle, may now be diagnosed using well-accepted criteria. Right ventricular infarction is clearly associated with anterior left ventricular infarction as well as inferior infarction. It may occur in 30% to 40% of patients with inferior infarction, although a much smaller percentage experience hemodynamic instability on the basis of right ventricular infarction. Pathophysiologically, right ventricular systolic and diastolic dysfunction are exacerbated by pericardial restraint and concomitant left ventricular dysfunction, accounting for the characteristic findings of cardiogenic shock and marked preload dependence in many patients. Right ventricular infarction may be suspected on the grounds of clinical presentation, physical examination, and enzymatic findings, and is confirmed using well-defined electrocardiographic, radionuclide, echocardiographic, and hemodynamic criteria. Once diagnosed, right ventricular infarction requires specific hemodynamic and pharmacologic management, including the judicious use of volume expansion and inotropic support. Several forms of mechanical and surgical intervention are of therapeutic value in treating hemodynamic disturbances and recognized complications. With appropriate management, the prognosis for patients with right ventricular infarction is generally favorable.

To improve the diagnosis and forecast the response to surgery or renal angioplasty in patients with hypertension and renal artery stenosis, we employed a simplified captopril renography protocol in conjunction with renal arteriography in 94 clinically selected patients. Fifty hypertensive patients (group 1) with a high clinical likelihood of renovascular hypertension were evaluated using a simplified captopril renography protocol and renal angiography on the arterial side. Criteria for normal captopril renal scintigrams were established based on this original cohort and validated in an additional 44 clinically comparable patients (group 2). Renal revascularization or nephrectomy was performed in 39 patients, and success of the procedure was determined in the 34 patients for whom 3-month follow-up was available. In the 94 patients, 44 (47%) had renal artery stenosis. Simplified captopril renography was 91% sensitive and 94% specific in identifying or excluding renal artery stenosis in the combined group, with no difference in the diagnostic utility between groups 1 and 2, or in those with renal insufficiency (n = 38) or those with bilateral disease (n = 17). Scintigraphic abnormalities induced by captopril were strongly associated with cure or improvement in blood pressure control following revascularization or nephrectomy (15 of 18), while the lack of captopril-induced changes was associated with failure of such intervention (13 of 16) (p = 0.0004). We conclude that simplified captopril renography is highly sensitive and specific in the diagnosis of renal artery stenosis in a clinically selected high-risk population and that the test accurately predicts the success or failure of therapeutic intervention.

Normal left ventricular systolic performance with impaired left ventricular diastolic filling may be present in a substantial number of patients with congestive heart failure (CHF). To evaluate the effect of oral verapamil in this subset, 20 men (mean age 68 +/- 5 years) with CHF, intact left ventricular function (ejection fraction greater than 45%) and abnormal diastolic filling (peak filling rate less than 2.5 end-diastolic volumes per second [edv/s]) were studied in a placebo-controlled, double-blind 5-week crossover trial. All patients underwent echocardiography to rule out significant valvular disease, and thallium-201 stress scintigraphy to exclude major active ischemia. Compared to baseline values, verapamil significantly improved exercise capacity by 33% (13.9 +/- 4.3 vs 10.7 +/- 3.4 minutes at baseline) and peak filling rate by 30% (2.29 +/- 0.54 vs 1.85 +/- 0.45 edv/s at baseline) (all p less than 0.05). Placebo values were 12.3 +/- 4.0 minutes and 2.16 +/- 0.48 edv/s, respectively (difference not significant for both). Improvement from baseline in an objective clinico-radiographic heart failure score (scale 0 to 13) was significantly greater with verapamil compared to placebo (median improvement in score: 3 vs 1, p less than 0.01). Mean ejection fraction and systolic blood pressure were unchanged from baseline; diastolic blood pressure and heart rate decreased to a small degree. Verapamil may have therapeutic efficacy in patients with CHF, preserved systolic function and impaired diastolic filling.

Despite increasing evidence favoring intensive therapy of high blood pressure (BP) (1, 2, 3, 4, 5), lower treatment goals have yet to be realized in clinical practice. This chapter will explore the evolution of practice guidelines, with a focus on trial findings that demonstrate benefits of vigorous BP management, especially in the diabetic population. We will review pharmacologic strategies derived from clinical trials, with an emphasis on optimal treatment for hypertensives with and without diabetes.

Free wall rupture of the myocardium is an important complication and major cause of death following acute transmural (ST segment elevation) myocardial infarction. Pathologic changes on a cellular level may combine with mechanical stressors to weaken the myocardium postinfarction. Risk factors for myocardial rupture include advanced age, female gender, prior hyper-tension, first myocardial infarction, late presentation, lack of collateral blood flow, and persisting chest pain and ST segment elevations. Thrombolytic therapy does not increase risk of rupture when given early in myocardial infarction, but late thrombolytic therapy may heighten risk. Primary percutaneous coronary intervention for acute myocardial infarction has reduced the incidence of myocardial rupture compared to thrombolytic therapy. This advantage likely can be ascribed to higher rates of immediate reperfusion with catheter techniques, as well as to the avoidance of thrombolytic-mediated hemorrhagic transformation of the infarction zone. Careful regulation of blood pressure and pulse using nitrates and beta-adrenergic blockers may mitigate the tendency toward myocardial rupture. Early and accurate diagnosis based on clinical and echocardiographic evidence can lead to successful surgical treatment.

Thiazolidinediones (TZDs) and metformin are insulin-sensitizing antihyperglycemic agents with reported benefits on atherosclerosis. Despite extensive use in patients with diabetes and cardiovascular disease, there is a paucity of outcomes data with metformin and none yet with TZDs. We sought to determine the impact of these insulin sensitizers on outcomes in diabetic patients after hospitalization with acute myocardial infarction (AMI).We conducted a retrospective cohort study of 24,953 Medicare beneficiaries with diabetes discharged after hospitalization with AMI between April 1998 and March 1999 or July 2000 and June 2001. The independent association between discharge prescription for metformin, TZD, or both agents and outcomes at 1 year was assessed in multivariable Cox proportional hazards models, adjusting for patient, physician, and hospital variables. The primary outcome was time to death within 1 year of discharge; secondary outcomes were time to first rehospitalization within 1 year of discharge for AMI, heart failure, and all causes.There were 8,872 patients discharged on an antihyperglycemic agent, of which 819 were prescribed a TZD, 1,273 metformin, and 139 both drugs. After multivariable analysis, compared with patients prescribed an antihyperglycemic regimen that included no insulin sensitizer, mortality rates were not significantly different in patients treated with either metformin (hazard ratio [HR] 0.92 [95% CI 0.81-1.06]) or a TZD (0.92 [0.80-1.05]) but were lower in those prescribed both drugs (0.52 [0.34-0.82]). The results were similar among patients with heart failure. The prescription of a TZD was associated with a borderline higher risk of all-cause readmission (1.09[1.00-1.20]), predominately due to a higher risk for heart failure readmission (1.17 [1.05-1.30]).Individually, prescription of insulin-sensitizing drugs is not associated with a significantly different risk of death in older diabetic patients within 1 year following AMI compared with other antihyperglycemic agents. Combined, however, metformin and TZDs may exert benefit. TZD prescription is associated with a higher risk of readmission for heart failure after myocardial infarction.

Recurrent stroke is a major public health concern and new treatment strategies are needed. While modulation of the renin angiotensin aldosterone system (RAAS) has proven effective in reducing recurrent cardiac events, its role in preventing recurrent cerebrovascular events remains unclear. RAAS is both a circulating and tissue based hormonal system that regulates homeostasis and tissue responses to injury in both the CNS and the periphery, via the activity of angiotensin II (Ang II). Vascular and hematologic effects induced by Ang II including endothelial dysfunction, vascular structural changes, inflammation, hemostasis, and fibrinolysis are increasingly linked to the occurrence of cerebrovascular events. Animal models have shown that RAAS modulation may be protective in cerebrovascular disease. The HOPE and LIFE trials support the role of blood pressure independent mechanisms of RAAS modulation for improving outcomes in a broad range of patients with cardiovascular disease but do not specifically address recurrent stroke prevention. PROGRESS, a trial of secondary stroke prevention, demonstrates that blood pressure reduction with a combination strategy including the routine use of ACE inhibitors prevents recurrent stroke. Current evidence suggests that the RAAS plays an important role in the development and progression of cerebrovascular disease. Modulation of the RAAS holds promise for the secondary prevention of stroke, however, ongoing clinical trials will better define the exact role of ACE inhibitor and angiotensin II Type 1 receptor blocker therapy in stroke survivors.

ContextAccording to package inserts, metformin is contraindicated in diabetic patients receiving drug treatment for heart failure therapy, and thiazolidinediones are not recommended in diabetic patients with symptoms of advanced heart failure. Little is known about patterns of use of these antihyperglycemic drugs in diabetic patients with heart failure.ObjectiveTo determine the proportions of patients hospitalized with heart failure and concomitant diabetes treated with metformin or thiazolidinediones.DesignSerial cross-sectional measurements using data from retrospective medical record abstraction.SettingNongovernmental acute care hospitals in the United States.PatientsTwo nationally representative samples of Medicare beneficiaries hospitalized with the primary diagnosis of heart failure and concomitant diabetes between April 1998 and March 1999 and between July 2000 and June 2001.Main Outcome MeasuresThe prescription of either metformin or a thiazolidinedione at hospital discharge.ResultsIn the 1998-1999 sample (n = 12 505), 7.1% of patients were discharged with a prescription for metformin, 7.2% with a prescription for a thiazolidinedione, and 13.5% with a prescription for either drug. In the 2000-2001 sample (n = 13 158), metformin use increased to 11.2%, thiazolidinedione use to 16.1%, and use of either drug to 24.4% (P

The renin-angiotensin-aldosterone system (RAAS) exerts a principal influence in maintaining vascular tone, optimal salt and water homeostasis, and forward cardiac output in human beings. Overactivity of the RAAS can lead to pathologic consequences in states of diabetic nephropathy, hypertension, renal artery stenosis, left ventricular hypertrophy, coronary atherosclerosis, myocardial infarction, and congestive heart failure. In addition to fluid and hemodynamic effects, the RAAS may have a critical role in the activation of the sympathetic nervous system, the progression of atherosclerosis, the dysregulation of endothelial function, and the inhibition of the fibrinolytic system. Accumulated basic and clinical evidence supports the use of inhibitors of the RAAS, including aldosterone antagonists, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers, in treating hypertension, improving diabetic nephropathy, preventing or ameliorating congestive heart failure, and optimizing the prognosis after myocardial infarction.

Pulse pressure has been related to higher risk of cardiovascular events in older persons. Isolated systolic hypertension is common among the elderly and is accompanied by elevated pulse pressure. Treatment of isolated systolic hypertension may further increase pulse pressure if diastolic pressure is lowered to a greater extent than systolic pressure. Little is known regarding pulse pressure as a predictor of cardiovascular outcomes in elderly persons with isolated systolic hypertension, and the influence of treatment on the pulse pressure effect. We assessed the relation between pulse pressure, measured throughout the follow-up period, and the incidence of coronary heart disease (CHD), heart failure (HF), and stroke in 4,632 participants in the Systolic Hypertension in the Elderly Program, a 5-year randomized, placebo-controlled clinical trial of treatment of isolated systolic hypertension in older adults. In the treatment group, a 10-mm Hg increase in pulse pressure was associated with a statistically significant 32% increase in risk of HF and a 24% increase in risk of stroke after controlling for systolic blood pressure and other known risk factors, as well as with a 23% increase in risk of HF and a 19% increase in risk of stroke after controlling for diastolic blood pressure and other risk factors. Pulse pressure was not significantly associated with HF or stroke in the placebo group, nor with incidence of CHD in either the placebo or treatment group. These results suggest that pulse pressure is a useful marker of risk for HF and stroke among older adults being treated for isolated systolic hypertension.

Hypertension is the most common reason for adult medical office visits in the U.S. today. With increasing longevity, an aging population, a greater prevalence of obesity, and a falling threshold for indications for high blood pressure treatment, the diagnostic evaluation of the hypertensive patient assumes a major role in office practice. The majority of patients who are being assessed for newly discovered hypertension will benefit from a relatively simple evaluation without the use of high cost procedures. Evaluation includes a careful history for both blood pressure related findings and other cardiovascular risk factors, a physical examination aimed at identifying possible specific etiologies and target organ damage, as well as some basic laboratory assays. In a rapid and relatively inexpensive fashion, the patient then can be directed toward nonpharmacologic treatment, drug therapy, or more specialized investigations as needed. (c)2000 by Le Jacq Communications, Inc.

For the purposes of this chapter, treatment of mitral valve disease is divided into medical management, catheter valvuloplasty, and surgical techniques. Treatments are divided into those for mitral stenosis and those for mitral regurgitation. Specific attention is paid at the conclusion of this chapter to the issues of the results of mitral valve surgery (especially as regards ventricular function and patient outlook), the complications of mitral valve surgery, the controversies of repair versus replacement, and chordal division versus preservation, and the issue of mitral valve surgery in the “bad” ventricle.

The functional mitral valve apparatus comprises the mitral annulus, the mitral leaflets, the chordae tendineae, the papillary muscles, and the adjacent atrial and ventricular myocardium. Abnormalities in one or more of these structures can lead to mitral regurgitation (MR) (Figure 23.1). Mitral regurgitation can be defined as retrograde flow of blood from the left ventricle to the left atrium as a consequence of inadequate closure of the mitral leaflets. The incidence of chronic MR is difficult to ascertain accurately because the condition frequently remains asymptomatic until late in its course. It is often detected on routine physical examination. In the United States, mitral valve prolapse and coronary artery disease account for the majority of cases of MR.