Biomedical subjects
Publications and source records attributed to M A Alpert.
Longer duration of morbid obesity is associated with higher LV mass, poorer LV systolic function, and greater impairment of LV diastolic filling. Weight loss-induced decreases in LV mass and improvements in LV systolic function and diastolic filling are due in part to favorable alterations in LV loading conditions.
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To identify factors influencing left ventricular (LV) diastolic filling in patients with morbid obesity, we performed transthoracic and Doppler echocardiography on 50 subjects whose actual body weight was > or = twice their ideal body weight and on 50 normal lean control subjects. The transmitral Doppler E/A ratio and E wave deceleration half-time were used to assess LV diastolic filling. Significant negative correlations were seen between the E/A ratio and the LV internal dimension in diastole (r = 0.819, p = 0.0001), systolic blood pressure (r = 0.751, p = 0.0001), LV end-systolic wall stress (r = 0.782, p = 0.0001), and LV mass/height index (r = 0.901, p = 0.0001). Significant positive correlations were seen between the E wave deceleration half-time and the LV internal dimension in diastole (r = 0.743, p = 0.0001), systolic blood pressure (r = 0.789, p = 0.0001), LV end-systolic wall stress (r = 0.828, p = 0.0001), and LV mass/height index (r = 0.831, p = 0.0001). No correlation was seen between diastolic blood pressure and either index of LV diastolic filling. Thus increasing LV mass is associated with progressive impairment of LV diastolic filling in morbidly obese individuals. The aforementioned alterations in LV loading conditions may contribute to impairment of LV diastolic filling directly or by increasing LV mass.
OBJECTIVE: To determine the interrelationship of left ventricular (LV) mass, systolic function and diastolic relaxation in morbidly obese subjects. METHOD: We obtained echocardiograms (M-mode, two dimension) and cardiac Doppler studies (pulse wave, continuous wave colour flow) on 50 subjects whose actual body weight was > or = twice ideal body weight. LV mass/height index was calculated from echocardiographic data (Penn Convention). LV systolic function was assessed by calculating LV fractional shortening. LV diastolic filling was assessed by measuring the transmitral Doppler E/A ratio and the transmitral E wave deceleration time. RESULTS: There were significant positive correlations between LV mass/height index and the LV internal dimensions in diastole, systolic blood pressure, LV end-systolic wall wall stress and the transmitral E wave deceleration time. There were significant negative correlations between LV mass/height index and both LV fractional shortening and the transmitral Doppler E/A ratio. There were significant negative correlations between LV fractional shortening and the LV internal dimension in diastole, systolic blood pressure LV end-systolic wall stress and the transmitral E wave deceleration time. There was a significant positive correlation between LV fractional shortening and the transmitral Doppler E/A ratio. There were significant positive correlations between the transmitral E wave deceleration time and LV internal dimension in diastole, systolic blood pressure and LV end-systolic wall stress. There were significant negative correlations between the transmitral Doppler E/A ratio and the aforementioned variables. CONCLUSIONS: Unfavourable alterations in LV loading conditions contribute to the development of LV hypertrophy and impairment systolic dysfunction in morbidly obese subjects. Increasing LV mass and altered loading conditions may synergistically contribute to impairment of LV diastolic filling in such individuals.
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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 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.
To determine whether obvious hemodynamic advantages of continuous ambulatory peritoneal dialysis (CAPD) over intermittent hemodialysis are reflected in superior cardiac structure and function, 16 of 55 analyzed CAPD patients (CAPD duration: 28 months) were followed over 35 months with echocardiography in a prospective analysis: 26 patients had died. LV dimensions (end-diastolic: 52 +/- 7 vs. 51 +/- 8 mm; control vs. follow-up) and systolic function (ejection fraction: 63 +/- 10 vs. 59 +/- 14%) were normal. Major findings were an increase in the amount of initially observed LV hypertrophy (251 +/- 68 vs. 342 +/- 135 g; p less than 0.03) and a decrease in mean LV volume/mass ratios (0.73 +/- 0.17 vs. 0.54 +/- 0.13; p less than 0.001). Excluding patients with dilated cardiomyopathy and valve disease, the amount of progression in LV hypertrophy was related directly to mean arterial pressure and cardiac output (n = 12; p less than 0.02) despite extensive use of antihypertensive medication (1.9 +/- 1.3 vs. 1.5 +/- 1.4 drugs/patient). No correlation was found with diastolic blood pressure, hemoglobin, serum parathyroid hormone, creatinine, urea, age, or CAPD duration. We conclude that LV hypertrophy is frequent in CAPD patients and further increases during long-term CAPD treatment. Factors contributing to the progression of LV hypertrophy are hypertension and hypercirculation.
Ten patients with pulmonary hypertension associated with diffuse systemic sclerosis (1 patient), the CREST syndrome (calcinosis cutis, Reynaud's phenomenon, esophageal dysmotility, sclerodactyl, telangiectasia) (6 patients) and mixed connective tissue disease (3 patients) were studied to assess the effect of oral nifedipine on pulmonary and systemic hemodynamics. Each patient underwent right-sided cardiac catheterization just before nifedipine administration. Thereafter, oral nifedipine was administered in 10 mg increments every 90 minutes until pulmonary vascular resistance normalized or a total dose of 30 mg was achieved. Hemodynamic measurements were obtained at 30-minute intervals for 3 hours, then hourly for 9 hours (acute study). Hemodynamic studies were repeated 3 to 6 months after the initial catheterization with the minimum dose of oral nifedipine (administered every 8 hours) required to achieve maximal reduction of pulmonary vascular resistance in the acute study (long-term study). In the acute study, oral nifedipine produced a significant decrease in mean pulmonary vascular resistance from 6.3 +/- 3.8 to 4.3 +/- 3.6 U (p less than 0.001). Similar changes in pulmonary vascular resistance were noted in the long-term study (n = 6). The results indicate that oral nifedipine is capable of producing an acute and sustained reduction in pulmonary vascular resistance in patients with pulmonary hypertension associated with diffuse systemic sclerosis, the CREST syndrome and mixed connective tissue disease.
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Mitral valve prolapse is a common cardiac disorder that can readily be diagnosed by characteristic auscultatory and echocardiographic criteria. Although many diseases have been associated with mitral valve prolapse, most affected individuals have the primary form of the disorder. Mitral valve prolapse is an inherited condition commonly associated with myxomatous degeneration of the mitral valve and its support structures. Complications of mitral valve prolapse, including cardiac arrhythmias, sudden death, infective endocarditis, severe mitral regurgitation (with or without chordae tendineae rupture), and cerebral ischemic events, occur infrequently considering the wide prevalence of the disorder. Panic disorder is a specific type of anxiety disorder characterized by at least three panic attacks within a 3-week period or one panic attack followed by fear of subsequent panic attacks for at least 1 month. It too is a common condition with a prevalence and age and gender distribution similar to that of mitral valve prolapse. Panic disorder and mitral valve prolapse share many nonspecific symptoms, including chest pain or discomfort, palpitations, dyspnea, effort intolerance, and pre-syncope. Chest pain is the symptom in both conditions that most commonly brings the patient to medical attention. The clinical description of chest pain in patients with mitral valve prolapse is highly variable, possibly reflecting multiple etiologies. Chest pain in panic disorder is usually characterized as atypical angina pectoris and as such bears resemblance to the chest pain commonly described by patients with mitral valve prolapse. Multiple investigative attempts to elucidate the mechanism of chest pain in both conditions have failed to identify a unifying cause. Review of the literature leaves little doubt that mitral valve prolapse and panic disorder frequently co-occur. Given the similarities in their symptomatology, a high rate of co-occurrence is, in fact, entirely predictable. There is, however, no convincing evidence of a cause-effect relationship between the two disorders, nor has a single pathophysiologic or biochemical mechanism been identified that unites these two common conditions. Until specific biologic markers for these disorders are identified, it may be impossible to do so. The lack of a proven cause-and-effect relationship between mitral valve prolapse and panic disorder and the absence of a unifying mechanism do not diminish the clinical significance of the high rate of co-occurrence between the two conditions. Primary care physicians and cardiologists frequently encounter patients with mitral valve prolapse and nonspecific symptoms with no discernible objective cause who fail to respond to beta-blockade. Panic disorder should be considered as a possible explanation for symptoms in such patients.(ABSTRACT TRUNCATED AT 400 WORDS)
A terminal QRS deflection on a 12-lead electrocardiogram (previously described as peri-infarction block) most likely represents slowed conduction in a large area of myocardium near the infarct zone. We have described a patient with peri-infarction block, abnormal findings on signal-averaged electrocardiogram, and reentrant ventricular tachyarrhythmias. Our observation underscores the need to recognize the importance of terminal QRS deflections in the appropriate clinical situation.
To assess the effect of hemodialysis on the left ventricular (LV) systolic function in the presence and absence of beta blockade, we performed echocardiography just prior to and immediately after 4-hour maintenance hemodialysis in 38 patients with end-stage renal disease. The LV systolic function was assessed in subgroups with normal and increased LV mass in both the beta blockade group (n = 19) and the non-beta blockade group (n = 19). There was a significant negative correlation between LV mass and the dialysis-induced change in the mean velocity of LV circumferential fiber shortening (mean Vcf) in both the beta blockade group (r = -0.93; p less than 0.0005) and in the non-beta blockade group (r = -0.82; p less than 0.0005). The mean dialysis-induced change in mean Vcf in the subgroup with increased LV mass in the beta blockade group (-0.02 +/- 0.11 circumferences/s) was significantly lower than the mean dialysis-induced change in mean Vcf in the non-beta blockade group (+0.12 +/- 0.04 circumferences/s; p less than 0.0005). Thus, the coexistence of increased LV mass and beta blockade significantly impedes the expected improvement of LV systolic function associated with hemodialysis.
Coronary artery aneurysms are detected with increasing frequency owing to the advent of coronary angiographies. Although most patients with coronary artery aneurysms are asymptomatic, manifestations of myocardial ischemia may occur. The case described herein serves as a basis for a discussion of the pathogenesis, clinical manifestations, detection, and treatment of coronary artery aneurysms.
To assess the efficacy of oral betaxolol in the treatment of stable exertional angina pectoris and to determine the relationship between betaxolol doses/serum concentrations and clinical/hemodynamic responses the authors studied 24 patients prior to and following stepwise administration of 5, 10, 20, 40, and 80 mg doses. The major endpoint for the study was the achievement of clinical beta blockade (heart rate 50-60 beats/min and less than or equal to 20% rise in treadmill stage I heart rate). Betaxolol produced a decrease in mean angina pectoris frequency from 6.6 +/- 1.9 episodes/week with placebo to 0.2 +/- 0.5 episode/week during clinical beta blockade (p less than 0.00005). Mean treadmill exercise time increased from 3.1 +/- 1.7 min with placebo to 7.3 +/- 2.3 min with doses sufficient to reduce angina pectoris frequency greater than or equal to 75% (p less than 0.00005) and to 8.0 +/- 2.3 min during clinical beta blockade (p less than 0.00005). The mean doses of betaxolol required to produce a greater than or equal to 75% decrease in angina pectoris frequency and clinical beta blockade were 12 +/- 5 mg (range 5-40 mg) and 28 +/- 29 mg (range 5-80 mg) respectively. Mean serum concentrations associated with these clinical endpoints were 23.8 +/- 9.7 ng/mL and 59.7 +/- 54.0 ng/mL respectively. The results indicate that betaxolol, in widely ranging doses, is highly effective in reducing angina pectoris frequency and improving exercise capacity in patients with stable exertional angina pectoris.
To assess the effect of exercise and to determine the influence of the right ventricular (RV) internal dimension on RV systolic function in morbid obesity, M-mode and 2-dimensional echocardiography and radionuclide ventriculography were performed on 22 patients whose body weight was at least twice the ideal body weight and who had no clinical or laboratory evidence of underlying organic heart disease or pulmonary disease. RV ejection fraction was measured at rest and during peak supine bicycle exercise. RV exercise response was defined as the change in RV ejection fraction during peak exercise. There was a significant negative correlation between percent over ideal body weight and RV exercise response (r = 0.86, p less than 0.00005) and between RV internal dimension and RV exercise response (r = 0.60, p less than 0.005). There were significant positive correlations between resting RV and left ventricular (LV) ejection fraction (r = 0.56, p less than 0.01) and between RV and LV exercise response (r = 0.70, p less than 0.0005). The subgroup with a high-normal or enlarged RV internal dimension (greater than or equal to 2.0 cm, n = 10) experienced no significant change in RV ejection fraction with exercise, whereas the subgroup whose RV internal dimension was less than 2.0 (n = 12) experienced a significant increase in RV ejection fraction from 44 +/- 10% at rest to 58 +/- 11% at peak exercise (p less than 0.03). The results suggest that in morbidly obese individuals without underlying cardiopulmonary disease RV dilatation may predispose to RV systolic dysfunction and assessment of RV systolic function should optimally include evaluation of RV exercise response.
To assess the effect of exercise on left ventricular (LV) systolic function and reserve in morbid obesity, radionuclide left ventriculography was performed before and during supine, symptom-limited bicycle exercise in 23 patients whose body weight was greater than or equal to twice their ideal body weight. Echocardiography was performed before exercise. Resting LV ejection fraction was depressed in 13 patients and LV mass was increased in 10 patients. Exercise produced nonsignificant increases (of similar magnitude) in mean LV ejection fraction in the subgroups with normal and depressed resting LV ejection fraction. Exercise produced a significant increase in LV ejection fraction from 54 +/- 8 to 65 +/- 12% (p less than 0.005) in the subgroup with normal LV mass, but produced no significant change in LV ejection fraction in the subgroup with increased LV mass (53 +/- 10 at rest, 50 +/- 12% during exercise). Moreover, the LV exercise response (change in LV ejection fraction during exercise) in the subgroup with normal LV mass was significantly different from that in the subgroup with increased LV mass (p less than 0.005). There was a strong positive correlation between LV mass and the percent over ideal body weight (r = 0.912, p = 0.01) and a strong negative correlation between LV mass and LV exercise response (r = 0.829, p = 0.01). The results suggest that increased LV mass predisposes morbidly obese patients to impairment of LV systolic function during exercise.
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