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Background: The prevalence and prognosis of previously undiagnosed angina pectoris (AP) in the absence of established cardiovascular disease (CVD) are unknown. This study sought to determine the prevalence and prognosis of previously undiagnosed AP in the absence of established CVD in the United States., Methods: Data derived from the National Health and Nutrition Examination Survey (2001-2018) and the Rose Angina Questionnaire (RAQ) were used to identify AP among participants ≥ 40 years without established CVD. Determinants of previously undiagnosed AP (AP undiagnosed prior to RAQ analysis) and predictors of all-cause mortality were identified using multivariable logistic regression analysis and the Cox proportional hazard model., Results: Of the 27,506 participants eligible for analysis, 621 participants had previously undiagnosed AP. Thus, the prevalence of previously undiagnosed AP was 1.99% (95% CI 1.79-2.20). Female gender, poverty, < high school education, hypertension, cigarette smoking, and obesity were independent predictors of previously undiagnosed AP. All-cause mortality rates were 1.71 per 1000 person months for participants with previously undiagnosed AP and were 1.08 per 1000 person months to those without previously undiagnosed AP (p = 0.003)., Conclusions: The prevalence of previously undiagnosed AP in the United States is 1.99% in persons ≥ 40 years of age without established CVD. Previously undiagnosed AP in those without established CVD was an independent predictor of all-cause mortality., Competing Interests: Conflict of interests None., (Copyright © 2022 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Human laterality disorders comprise a group of diseases characterized by abnormal location (situs) and orientation of thoraco-abdominal organs and vessels across the left-right axis. Situs inversus totalis is mirror image reversal of thoraco-abdominal organs/great vessels. Situs ambiguus, better known as heterotaxy, is abnormal arrangement of thoraco-abdominal organs across the left-right axis excluding situs inversus totalis. Heterotaxy, also referred to as atrial or atrial appendage isomerism, is characterized by abnormal location of left-sided or right-sided organs with loss of asymmetry of normally paired asymmetric organs. It is associated with a variety of anomalies involving the heart, great vessels, lungs and intra-abdominal organs. Right and left atrial isomerism are associated with multiple complex congenital cardiac and vascular anomalies, many of which are lethal when untreated. Isomerism may also affect the lungs, spleen, liver, gall bladder, and intestines. Innovative surgical therapy of heterotaxy/isomerism has reduced early mortality and markedly improved long-term prognosis., Competing Interests: Declaration of Competing Interest None of the authors report conflicts of interest or competing interests., (Copyright © 2021 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Background: Mechanical circulatory support (MCS) devices are often deployed to treat patients with refractory cardiogenic shock, rapid deterioration of heart failure, and inotrope-dependent patients. Stroke is a common complication of MCS therapy. This study assesses the risk of stroke during the early post-heart transplantation (HT) period (days from successful HT to discharge or death) in patients who received MCS therapy leading to HT., Methods: Data were derived from the United Organ Sharing (UNOS) database. MCS modalities studied include left ventricular assist devices (LVAD), right ventricular assist devices (RVAD), biventricular ventricular assist devices (BiVAD), and extra-corporeal membrane oxygenation (ECMO). A multiple logistic regression model was used to determine the risk of stroke during the early post-HT period associated in patients treated with MCS leading to HT., Results: Between 1988 and 2014, 10,258 patients received MCS therapy leading to HT. Of these, 160 patients (1.96%) developed stroke during the early post-HT period. Multiple regression analysis showed that MCS modalities and associated odds ratios for early post-HT stroke and associated 95% confidence intervals were as follows: LVAD (1.44, 0.70-2.94), RVAD (2.89, 1.03-8.05, BiVAD (3.24, 1.15-9.10), ECMO (2.27 (1.17-4.40), and any MCS (1.60 (1.20-2.12)., Conclusions: With the exception of left ventricular assist devices, use of MCS modalities leading to HT is significantly and independently associated with stroke during the early post-HT period., Competing Interests: Conflicts of Interest None., (Copyright © 2021 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Overweight and obesity contribute to the development of cardiovascular disease (CVD) in general and coronary heart disease (CHD) in particular in part by their association with traditional and nontraditional CVD risk factors. Obesity is also considered to be an independent risk factor for CVD. The metabolic syndrome, of which central obesity is an important component, is strongly associated with CVD including CHD. There is abundant epidemiologic evidence of an association between both overweight and obesity and CHD. Evidence from postmortem studies and studies involving coronary artery imaging is less persuasive. Recent studies suggest the presence of an obesity paradox with respect to mortality in persons with established CHD. Physical activity and preserved cardiorespiratory fitness attenuate the adverse effects of obesity on CVD events. Information concerning the effect of intentional weight loss on CVD outcomes in overweight and obese persons is limited., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background: Obesity has been reported to be associated with delayed ventricular repolarization. The purpose of this study was to assess ventricular repolarization in normotensive severely obese subjects with and without heart failure (HF) and to assess the effect of weight loss on ventricular repolarization in such patients., Methods: Twenty-eight patients with and 39 patients without HF (body mass index ≥ 40 kg/m(2)) were studied before and after weight loss from bariatric surgery. Corrected QT interval (QTc) was measured on 12-lead electrocardiograms using Bazett's formula. QTc dispersion was calculated by subtracting the minimum from the maximum QTc on each 12-lead electrocardiogram. Electrocardiograms and transthoracic echocardiograms were performed preoperatively and at the nadir of postoperative weight loss., Results: Mean QTc and QTc dispersion were significantly longer/greater in subjects with HF than in those without HF (P < 0.0001). Weight loss produced significant reductions in mean QTc and QTc dispersion in both subgroups (P < 0.0001). Pre-weight loss left ventricular (LV) mass/height and presence or absence of HF independently predicted pre-weight loss QTc and QTc dispersion (P < 0.0001). Weight loss-induced decrease in LV mass/height independently predicted weight loss-induced decreases in QTc and QTc dispersion (P < 0.0001)., Conclusions: HF independently predicts QTc and QTc dispersion in normotensive severely obese patients. Decrease in the LV mass resulting from weight loss independently predicts reduction in QTc and QTc dispersion in such patients.

Obesity is a risk factor for heart failure (HF) in both men and women. The mortality risk of overweight and class I and II obese adults with HF is lower than that of normal weight or underweight adults with HF of comparable severity, a phenomenon referred to as the obesity paradox. Severe obesity produces hemodynamic alterations that predispose to changes in cardiac morphology and ventricular function, which may lead to the development of HF. The presence of systemic hypertension, sleep apnea, and hypoventilation, comorbidities that occur commonly with severe obesity, may contribute to HF in such patients. The resultant syndrome is known as obesity cardiomyopathy. Substantial weight loss in severely obese persons is capable of reversing most obesity-related abnormalities of cardiac performance and morphology and improving the clinical manifestations of obesity cardiomyopathy., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Heart failure (HF) with a normal left ventricular (LV) ejection fraction (HFNEF) occurs in 40-71% of patients with HF and carries a prognosis similar to that of HF with a reduced LV ejection fraction (LVEF). The pathophysiology of HFNEF is distinct from that of HF with a reduced LVEF and is characterized by impaired relaxation of myocardium, LV stiffness and, in many cases, increased arterial stiffness. Systemic hypertension accounts for most cases of HFNEF in the United States. Those with HFNEF tend to be older and obese. Diabetes mellitus and atrial fibrillation occur with disproportionately high frequency in HFNEF. The diagnosis of HFNEF requires the presence of symptoms or signs of HF, a normal or near-normal LVEF and evidence of LV diastolic dysfunction based on cardiac catheterization or Doppler echocardiographic techniques and/or elevation of plasma natriuretic peptide levels. Current guidelines for management of HFNEF include control of systolic and diastolic hypertension, control of the ventricular rate in patients with atrial fibrillation and judicious use of diuretics. In selected cases, coronary revascularization or restoration of sinus rhythm in those with atrial fibrillation may be indicated. To date, no drug or drug group has consistently improved survival in HFNEF. For this reason and because of the poor long-term prognosis, preventative measures and effective treatment of underlying causes and precipitating factors are particularly important in avoiding HF exacerbations in patients with HFNEF.

Obesity has reached epidemic proportions in the United States and worldwide. Considering the adverse effects of obesity on left ventricular (LV) structure, diastolic and systolic function, and other risk factors for heart failure (HF), including hypertension and coronary heart disease, HF incidence and prevalence, not surprisingly, is markedly increased in obese patients. Nevertheless, as with most other cardiovascular diseases, numerous studies have documented an obesity paradox, in which overweight and obese patients, defined by body mass index, percent body fat, or central obesity, demonstrate a better prognosis compared with lean or underweight HF patients. This review will describe the data on obesity in the context of cardiopulmonary exercise testing in HF. Additionally, the implications of obesity on LV assist devices and heart transplantation are reviewed. Finally, despite the obesity paradox, we address the current state of weight reduction in HF., (Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: The lungs of patients with pulmonary arterial hypertension (PAH) exhibit decreased bioavailability of nitric oxide and downstream signaling through cyclic guanosine monophosphate (cGMP). Therapies that enhance cGMP-mediated vasodilation have shown efficacy in treating PAH. We tested the hypothesis that combination therapy with sildenafil, a cGMP phosphodiesterase type 5 inhibitor, and brain natriuretic peptide (BNP), a receptor-mediated guanosine cyclase stimulator, synergistically attenuates monocrotaline-induced PAH in rats compared with either monotherapy., Methods: Adult male Sprague-Dawley rats were subcutaneously injected with monocrotaline (n = 41, 50 mg/kg). After approximately 4 weeks, the rats were infused intravenously with vehicle solution, sildenafil (42 and 85 microg/kg/min), or BNP (50 and 100 ng/kg/min), alone and in varied combination. The primary endpoint was the relative change in right ventricular systolic pressure (RVSP) and mean arterial systemic pressure (MAP). Secondary endpoints included heart rate and dP/dt., Results: Vehicle infusions did not alter hemodynamic variables. Sildenafil85 (85 microg/kg/min) alone decreased RVSP (-16.6 +/- 5.6%) and decreased MAP (-4.0 +/- 4.7%). BNP50 (50 ng/kg/min) and BNP100 (100 ng/kg/min) decreased RVSP (-23.3 +/- 5.7% and -27.1 +/- 2.9%, respectively) and MAP (-6.4 +/- 5.8% and -14.3 +/- 4.1%, respectively). Combination therapy with sildenafil42 and BNP50 decreased RVSP (-20.7 +/- 5.6%) and showed a lessened systemic effect (MAP = -11.6 +/- 5.9%). Combination therapy with sildenafil85 and BNP100 decreased RVSP (-27.6 +/- 3.2%, P = NS) and showed increased systemic effect (MAP = -20.7 +/- 3.1%, P < 0.05) in comparison with sildenafil85., Conclusions: This study suggests that intravenous administration of both sildenafil and BNP monotherapy produces significant improvement in RVSP, making them potentially viable options for the treatment of PAH, whereas combination therapy produces no additional improvement in pulmonary hemodynamics.

Infective endocarditis with Fusobacterium necrophorum (F necrophorum) as the sole pathogen has been reported only once previously in an infant. We describe herein a case of F necrophorum endocarditis in a 20-year-old, previously healthy man. This is the first reported case of monomicrobial F necrophorum endocarditis in an adult.

Background: Hyperglycemia commonly occurs in critically ill patients, even in the absence of diabetes mellitus, and is associated with increased morbidity and mortality rates in such patients., Methods: Medline search using the terms intravenous insulin, intensive care, myocardial infarction, cardiac surgery and stroke., Results and Conclusions: Intravenous insulin therapy with or without adjunctive subcutaneous insulin therapy has been shown to improve morbidity and reduce mortality rates in surgical intensive care populations compared with subcutaneous insulin alone or oral hypoglycemic therapy. The evidence for such is less compelling in medical intensive care populations. Intravenous insulin therapy alone or in combination with glucose and potassium infusion appears to improve clinical outcomes in cardiac surgery patients, but there is conflicting evidence concerning its effect on morbidity and mortality rates after myocardial infarction. Insufficient evidence exists to determine the effect of intravenous insulin therapy on outcomes in other populations including stroke patients, those undergoing major noncardiac surgery, and burn patients. Intravenous insulin nomograms and nurse-driven protocols may improve blood glucose control, resulting in improved clinical outcomes.

The metabolic syndrome is most commonly defined as the presence of three or more of the following atherogenic risk factors: increased abdominal waist circumference, hypertriglyceridemia, low serum high-density lipoprotein level, raised blood pressure, and a fasting blood sugar level greater than 110 mg/dL. It is associated with increased risk for the development of atherosclerosis and cardiovascular disease. Current management recommendations promote therapeutic lifestyle changes (mainly diet and exercise) for all of the core elements of the syndrome. Pharmacologic therapy is indicated in most patients with atherogenic dyslipidemia and in some with hyperglycemia and raised blood pressure. These therapeutic measures are able to favorably modify the core components of the metabolic syndrome and it is hoped that they will also improve the long-term cardiovascular prognosis in patients with this disorder.

Metabolic syndrome includes a clustering of metabolic derangements that cause affected subjects to have an increased risk for developing diabetes, cardiovascular disease, and, according to recent epidemiologic studies, chronic kidney disease. The present review discusses four definitions of metabolic syndrome published by different national and international committees. In an effort to bridge the differences existent in those classifications, a unified definition that recognizes the increased biologic activity of the upper visceral fatty tissue and the strong association of abdominal obesity as a leading part of metabolic syndrome is proposed herein. The diagnosis of metabolic syndrome is reserved for pre-diabetic patients who share the risk of becoming diabetic or developing cardiovascular or chronic kidney disease.

A 63-year-old man presented with ascites after therapy with amiodarone, 200 mg orally once per day for 22.5 months. A liver biopsy showed grade 3 chronic hepatitis and micronodular cirrhosis. The presence of striking microvesicular steatosis on light microscopy and lysosomal inclusion bodies on electron microscopy suggested amiodarone hepatotoxicity. This is the first reported case of amiodarone-induced hepatic cirrhosis associated with chronic treatment with 200 mg orally once per day for less than 2 years.

Granulomas have been described in a wide variety of organs in patients with Crohn disease, but not in spleen. This report describes a patient with noncaseating granulomas of the liver and spleen that responded promptly and fully to glucocorticoid therapy.

Pericardial involvement in end-stage renal disease (ESRD) is manifested most commonly as acute uremic or dialysis pericarditis and infrequently as chronic constrictive pericarditis. The causes of uremic and dialysis pericarditis remain uncertain. The clinical and laboratory manifestations of acute pericarditis, pericardial effusion, cardiac tamponade, and constrictive pericarditis in patients with chronic renal failure are similar to those observed in nonuremic patients with similar pericardial involvement, except that chest pain occurs less frequently in those with ESRD. Therapeutic interventions for acute uremic or dialysis pericarditis with or without pericardial effusion include intensive hemodialysis, pericardiocentesis (infrequently used), pericardiostomy with or without instillation of intrapericardial glucocorticoids, pericardial window, and pericardiectomy. Chronic constrictive pericarditis is treated with pericardiectomy.

Valvular and perivalvular involvement in end-stage renal disease (ESRD) is most commonly manifested as mitral annular calcification and aortic valve calcification. Both mitral and aortic valve calcification (MAC) occur more frequently and at younger age in those with ESRD than in those with normal renal function. Aortic valve calcification progresses to aortic stenosis more commonly and at a more accelerated rate than in the general population. Altered calcium and phosphate metabolism are thought to predispose to these valvular and perivalvular abnormalities. No treatment is necessary for MAC unless severe mitral regurgitation or stenosis occur (both are rare). Mitral valve repair or replacement and aortic valve replacement are indicated for severe symptomatic valve stenosis or regurgitation, albeit at a higher risk than in those with normal renal function. Infective endocarditis may complicate MAC or aortic stenosis in patients with ESRD and is associated with a high mortality rate in such patients.

Patients with end-stage renal disease (ESRD) experience a variety of hemodynamic and metabolic abnormalities that predispose to alterations in cardiac performance and morphology. High cardiac output related to renal anemia, hypertension, volume overload, and the arteriovenous fistula (in patients on hemodialysis) predispose to eccentric left ventricular (LV) hypertrophy. Hypertension, aortic stiffness, and aortic stenosis predispose to concentric LV hypertrophy. Most ESRD patients have a hybrid form of LV hypertrophy. LV hypertrophy is commonly accompanied by LV diastolic dysfunction. LV systolic dysfunction is less common. Newer dialytic techniques, excellent control of hypertension, and correction of renal anemia produce regression of LV hypertrophy. The effect of these interventions on LV systolic and diastolic function is less well established. Alterations in serum calcium, choice of dialysate base, hypoxia, and comorbid conditions may influence the effects of dialysis (particularly hemodialysis) on LV function. A variety of negative inotropic drugs may depress LV function in patients with ESRD.

A 54-year-old man developed unstable angina pectoris and was found to have both an anomalous left coronary artery, which arose from the right sinus of Valsalva and followed an intramyocardial (septal) course, and severe atherosclerotic stenosis of the mid-right coronary artery. Stress perfusion imaging showed ischemia in the distribution of the right coronary artery, leading to successful percutaneous transluminal balloon angioplasty of the right coronary artery rather than surgical correction of the congenital anomaly.

HELLP syndrome (hemolysis, elevation of liver enzymes, and low platelet count) occurs during pregnancy. Intrahepatic hemorrhage and subcapsular liver hematoma with or without rupture are reported complications of this syndrome. The patient described in this report developed HELLP syndrome associated with a subcapsular liver hematoma and pulmonary artery thrombus, complications that created a therapeutic conundrum.

Weight reduction diets may reduce the severity of risk factors for coronary heart disease such as diabetes mellitus, hypertension, and dyslipidemia. Several case reports and small studies of patients receiving starvation diets have reported hypotension and sudden cardiac death. Myofibrillar damage was documented in 1 case. Very-low-calorie diets are generally safe and well-tolerated. However, low QRS voltage, QT interval prolongation, and both nonsustained ventricular arrhythmias and sudden cardiac death have been described in subjects treated with such diets. Orthostatic hypotension may complicate very-low-calorie protein diets because of sodium depletion and depressed sympathetic nervous system activity. Bariatric surgery is associated with disproportionately high mortality rates in both the perioperative and postoperative periods.

Therapy of acute exacerbations of congestive heart failure associated with obesity cardiomyopathy consists of dietary salt restriction, inspired oxygen, diuretics, and angiotensin-converting enzyme inhibitors or, if left ventricular systolic dysfunction is present, hydralazine/isosorbide dinitrate. Digitalis may be indicated in selected cases. These measures may also be useful chronically in association with weight loss. Substantial weight loss is capable of reversing all of the hemodynamic abnormalities associated with obesity except elevation of left ventricular filling pressure. Substantial weight loss may also reduce left ventricular mass and improve left ventricular diastolic filling in those with left ventricular hypertrophy before weight loss. Left ventricular systolic function also improves after weight loss in those with impaired pre-weight-loss systolic function. These beneficial effects of weight loss occur partly because of favorable alterations in left ventricular loading conditions. Substantial weight loss in patients with congestive heart failure associated with obesity cardiomyopathy produces a reversal of many of the clinical manifestations of cardiac decompensation and improves New York Heart Association functional class in most patients.

Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/ obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death.

Background: Morbid obesity produces a variety of ECG alterations, including leftward shifts of the P-wave, QRS, and T-wave axes; disproportionately high frequencies of low QRS voltage; left ventricular hypertrophy and left atrial abnormality; and a high frequency of T-wave flattening in the inferior and lateral leads. This study was designed to assess the effects of substantial weight loss on the ECG in morbid obesity., Methods: We performed a resting 12-lead ECG on 60 normotensive patients (48 women and 12 men; mean +/- SD age, 37 +/- 7 years), whose body weight was twice their ideal body weight prior to and at the time of maximum weight loss after bariatric surgery., Results: Mean weight decreased from 136 +/- 7 to 85 +/- 3 kg. Weight loss produced significant decreases in the frequencies of low QRS voltage; Romhilt-Estes point score > or = 5 points; SV(1) + RV(5) or V(6) > 35 mm; RV(5) or V(6) > 26 mm; RaVL > 11 mm; RaVL > or = 7.5 mm; SaVR > 14 mm; P-terminal force more negative than - 0.04 mm.s in lead V(1); and T-wave flattening in the inferior, lateral, and inferolateral leads. Weight loss significantly shifted the mean P-wave, QRS, T-wave axes rightward, and significantly reduced mean RaVL and mean SaVR voltage., Conclusion: Substantial weight loss is capable of reversing many of the ECG alterations associated with morbid obesity.

Observational studies have found that estrogen replacement therapy (ERT) reduces the risk of coronary heart disease (CHD) in postmenopausal women. To determine the frequency of current use of ERT in an economically and racially diverse group of women at high risk for CHD, we examined the medical records of 393 women older than 40 who were admitted to the University of South Alabama Medical Center with symptoms suggestive of angina. Women in the study group were classified as African American or European American and data were examined for significant differences. Use of ERT was lower in African American women (11 of 111, 9.9%) than in European American women (26 of 152, 17.1%, odds ratio 1.9). Compared with the reported utilization of ERT in middle-class European American women, ERT is underutilized in this economically diverse group of women at high risk for coronary heart disease. In our population, European American women were twice as likely to be receiving ERT as African American women.

This case report describes a patient with hypertrophic cardiomyopathy who developed symptomatic atrial fibrillation on two occasions after ingesting sildenafil citrate (Viagra). Sildenafil citrate should be withheld or used with extreme caution in persons with hypertrophic obstructive cardiomyopathy.

Purpose: The purpose of this study is to determine whether short-term heart rate variability (HRV) can be used successfully to predict inducible ventricular tachycardia (VT)., Methods: A high-speed (300 mm/s) electrocardiographic recording was obtained in 32 patients in the supine position prior to programmed ventricular stimulation. Beat-to-beat RR intervals (in milliseconds) were derived from an 11-beat strip (10 RR intervals). Logistic regression was used to study the relationship between several variables and a dichotomous dependent variable (inducible, clinical, or electrocardiographic evidence of VT)., Results: Of 32 patients, 12 had inducible VT (inducible VT group) and 20 had no clinical or electrocardiographic evidence of VT (control group). Mean short-term HRV values were significantly lower in those with inducible VT than in the control group in all patients (25+/-15 ms, n=12 vs 67+/-22 ms, n=20; p<0.0001) and in patients with coronary artery disease or congestive heart failure or both (22+/-13 ms, n=11 vs 63+/-23 ms, n=11; p<0.0001). For the group as a whole, short-term HRV was < or =50 ms in 11 of 12 patients (92%) with inducible VT, but was < or =50 ms in only 3 of 20 control subjects (15%; p<0.001). As a result of a stepwise selection procedure conducted within the logistic regression, only the short-term HRV was found to be predictive of inducible VT (p<0.0001)., Conclusion: Short-term HRV is significantly lower in subjects with inducible VT than in those without clinical or electrocardiographic evidence of VT. The probability of developing sudden death increases substantially when short-term HRV decreases below 50 ms.

A 19-year-old man received a gunshot wound to the heart. Transthoracic echocardiography was unable to localize the bullet fragment, whereas transesophageal echocardiography localized the bullet fragment in the posteroseptal wall at the base of the posteromedial papillary muscle.

Obesity can result in alterations in cardiac structure and function even in the absence of systemic hypertension and underlying organic heart disease. Increased total blood volume creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular (LV) hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The presence of systemic hypertension in obese individuals facilitates development of LV dilatation and hypertrophy. Congestive heart failure may occur in such individuals, and may be attributable to LV diastolic dysfunction or to combined LV diastolic and systolic dysfunction. The sleep apnea/obesity hypoventilation syndrome occurs in 5% of morbidly obese individuals and is potentially life-threatening. Treatment of obesity cardiomyopathy consists of weight loss, salt restriction, and diuretics. Digitalis and vasodilators may be useful in selected cases. Central obesity is probably a risk factor for the development of coronary heart disease. Alterations in lipid and insulin metabolism may facilitate development of coronary heart disease in obese patients.

To assess the pulmonary and systemic hemodynamic effects of oral captopril in patients with connective tissue disease and pulmonary hypertension, we performed right heart catheterization in eight patients with diffuse systemic sclerosis, the CREST syndrome, or mixed connective tissue diseases prior to and immediately following administration of captopril (dose range 12.5 to 50.0 mg, short-term study). Four of these patients underwent repeat right heart catheterization after three to six months of oral captopril therapy (long-term study). In the short-term study, oral captopril produced a significant decrease in mean pulmonary vascular resistance from 6.2 +/- 3.6 to 4.6 +/- 3.8 units (p < 0.01). This was accompanied by a significant decrease in mean pulmonary artery pressure, mean blood pressure, mean systemic vascular resistance and a significant increase in cardiac output. Similar changes in pulmonary hemodynamics were noted in the long-term study. Thus, oral captopril is capable of producing an acute and sustained reduction in pulmonary vascular resistance in patients with pulmonary hypertension associated with the aforementioned connective tissue diseases.

This case report describes the evolution of an acute anteroseptal myocardial infarction in a 27-year-old man following intravenous injection of pentazocine and tripelennamine. Subsequent coronary angiography showed normal coronary arteries. Based on the known mechanism of action of these drugs, it is postulated that myocardial infarction resulted from coronary artery spasm secondary to excessive catecholamine stimulation.

To assess the comparative effects of hemodialysis with acetate versus bicarbonate base on left ventricular systolic function, we performed M-mode echocardiography on 36 patients prior to and immediately following 4-hr maintenance hemodialysis. Patients were initially dialyzed against either sodium acetate or sodium bicarbonate and 1 week later were dialyzed against the alternate base. The mean velocity of circumferential fiber shortening (mean Vcf, circumferences/s) was used to assess left ventricular systolic function. In patients with normal pre-dialysis mean Vcf hemodialysis with acetate produced no significant change in mean Vcf, whereas hemodialysis with bicarbonate produced a significant increase in mean Vcf. In patients with low pre-dialysis mean Vcf hemodialysis with either base produced a significant increase in mean Vcf. Mean Vcf values obtained after hemodialysis with bicarbonate were significantly higher than those obtained after hemodialysis with acetate, both in patients with normal and low pre-hemodialysis mean Vcf. We conclude that hemodialysis with bicarbonate produces a comparatively greater improvement in left ventricular systolic function than hemodialysis with acetate.

A 33-year-old man with no predisposing factors had a DeBakey type 1 aortic dissection requiring surgical intervention. Microscopic examination showed combined-type cystic medial necrosis. This is the first report of extensive aortic dissection associated with combined-type cystic medial necrosis in a person younger than 40 years with no predisposing factors.

To assess the effect of minoxidil on pulmonary hemodynamics, we performed cardiac catheterization on ten patients, prior to the administration of minoxidil, at six months after its addition to their existing drug regimens, and on seven patients following 12 or more months of minoxidil therapy. Systemic blood pressure and systemic vascular resistance were significantly reduced at six months and following 12 or more months of minoxidil therapy. Before receiving minoxidil, nine of ten patients had elevated pulmonary vascular resistance. There were no significant changes in pulmonary vascular resistance following the initiation of minoxidil. The data suggest that pulmonary hypertension is common in patients with long-standing poorly controlled systemic hypertension, and that minoxidil, in doses sufficient to significantly reduce systemic blood pressure, does not cause or aggravate pulmonary hypertension.

We performed M-mode echocardiography on 100 subjects with idiopathic mitral valve prolapse (IMVP) and on 100 normal control subjects to determine if differences exist between the two groups in cardiac chamber size, left ventricular performance or left ventricular mass. Subjects with IMVP demonstrated significantly greater left ventricular mass than normal control subjects. There were no significant differences in fractional shortening of the left ventricle or left ventricular end-diastolic volume. There was no significant difference in left ventricular mass between asymptomatic subjects with IMVP and those with chest pain, palpitations, syncope or presyncope. Subjects with and without mitral regurgitation showed no significant difference in mass. The results indicate that subjects with IMVP demonstrate subtle left ventricular hypertrophy which does not appear to be caused by underlying organic heart disease, mitral regurgitation or sustained hypercontractility. This suggests that myocardial involvement is an integral part of the IMVP syndrome.

The management of symptomatic bradyarrhythmias can be challenging in patients in whom cardiac pacing is not indicated, such as in the terminally ill or severely demented. We applied a transdermal scopolamine patch on one such patient with resultant substantial improvement in his supraventricular bradyarrhythmia.