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Biomedical subjects

M D Cheitlin

Publications and source records attributed to M D Cheitlin.

At least 19 recordsLinked to original sources

Pericardial effusion in AIDS. Incidence and survival.

BACKGROUND: Although pericardial effusion is known to be common among patients infected with HIV, the incidence of pericardial effusion and its relation to survival have never been described. METHODS AND RESULTS: To evaluate the incidence of pericardial effusion and its relation to mortality in HIV-positive subjects, 601 echocardiograms were performed on 231 subjects recruited over a 5-year period (inception cohort: 59 subjects with asymptomatic HIV, 62 subjects with AIDS-related complex, and 74 subjects with AIDS; 21 HIV-negative healthy gay men; and 15 subjects with non-HIV end-stage medical illness). Echocardiograms were performed every 3 to 6 months (82% had follow-up studies). Sixteen subjects were diagnosed with effusions (prevalence of effusion for AIDS subjects entering the study was 5%). Thirteen subjects developed effusions during follow-up; 12 of these were subjects with AIDS (incidence, 11%/y). The majority of effusions (80%) were small and asymptomatic. The survival of AIDS subjects with effusions was significantly shorter (36% at 6 months) than survival for AIDS subjects without effusions (93% at 6 months). This shortened survival remained significant (relative risk, 2.2, P = .01) after adjustment for lead time bias and was independent of CD4 count and albumin level. CONCLUSIONS: There is a high incidence of pericardial effusion in patients with AIDS, and the presence of an effusion is associated with shortened survival. The development of an effusion in the setting of HIV infection suggests end-stage HIV disease (AIDS).

AIDS-Related Complex

Coronary blood flow reserve in acute aortic regurgitation.

OBJECTIVES: This study sought to determine the impact of acute aortic regurgitation on coronary blood flow reserve and phasic epicardial coronary blood flow in closed-chest dogs. BACKGROUND: Hemodynamic changes in acute aortic regurgitation are known to precipitate myocardial ischemia. Coronary blood flow reserve has not been studied in closed-chest experimental preparations with acute aortic regurgitation. METHODS: Graded temporary acute aortic regurgitation was produced in 11 mongrel dogs. Phasic coronary blood flow velocities were measured using a Doppler guide wire. Coronary flow reserve was defined as the ratio of the time average of spectral peak velocity after administration of papaverine to that of the baseline state. RESULTS: Under control conditions (mean [+/- SEM] diastolic blood pressure 82.2 +/- 4.5 mm Hg), coronary flow reserve was 3.51 +/- 0.27 with predominantly diastolic epicardial coronary blood flow. With mild acute aortic regurgitation (diastolic blood pressure 61.8 +/- 3.0 mm Hg), coronary flow reserve decreased to 2.38 +/- 0.27, with an increase in phasic systolic epicardial coronary blood flow. At the onset of moderate acute aortic regurgitation (diastolic blood pressure 42.1 +/- 0.9 mm Hg), coronary flow reserve declined further to 1.46 +/- 0.12, and the phasic systolic epicardial coronary blood flow became more prominent. With severe aortic regurgitation (diastolic blood pressure 29.2 +/- 2.2 mm Hg), coronary flow reserve reached 1.20 +/- 0.05, and the phasic epicardial coronary blood flow pattern was found to be predominantly systolic with retrograde diastolic flow. The ratio of diastolic to systolic pressure-time indexes with severe aortic regurgitation suggested subendocardial underperfusion. CONCLUSIONS: This study demonstrates a marked decline in coronary blood flow reserve and documents a progressive change in the phasic epicardial blood flow to a predominantly systolic pattern with increasing degrees of acute aortic regurgitation.

Animals

Reappraisal of continuous positive airway pressure therapy in acute cardiogenic pulmonary edema. Short-term results and long-term follow-up.

To investigate whether serial incremental continuous positive airway pressure (CPAP) has any short-term or long-term advantages over face-mask oxygen therapy by way of intrapulmonary shunt reduction, 100 patients admitted to the coronary care unit for the treatment of acute cardiogenic pulmonary edema were studied. All patients received Swan-Ganz catheterization. Hemodynamic and pulmonary function parameters were recorded over the next 6 h, and the patients were followed until hospital discharge. All survivors received regular follow-up at 1-month intervals in the outpatient clinic. During the first-stage investigation period (3 h) PaO2 in the CPAP group showed a significant increase, whereas the intrapulmonary shunt and alveolar-arterial oxygen tension gradient (P[A-a]O2) was significantly reduced (p < 0.005). The CPAP group had significantly lower rate-pressure product and higher stroke volume index compared with the control group. The therapeutic failure rate over 6 h was 24% in the CPAP group and 50% in the control group (p < 0.01). The CPAP group had a significantly lower incidence of tracheal intubation and ventilator therapy than the control group; however, there was no significant difference in short-term mortality and hospital stay between the two groups. In conclusion, although study size was not large enough to demonstrate a difference in mortality, CPAP therapy resulted in physiologic cardiovascular and pulmonary function improvement and significantly reduced the need for intubation; however, it did not decrease mortality in patients with acute cardiogenic pulmonary edema, and a much larger study is needed to investigate this possibility.

Acute Disease

Vasodilator therapy in chronic asymptomatic aortic regurgitation: enalapril versus hydralazine therapy.

OBJECTIVES: This study attempted to evaluate the long-term efficacy of enalapril versus hydralazine therapy on left ventricular volume, mass and function as well as on the renin-angiotensin system in chronic asymptomatic aortic regurgitation. BACKGROUND: We tested the hypothesis that early administration of a vasodilator drug might be able to reduce left ventricular dilation and mass expansion. Because the renin-angiotensin system may be activated in chronic aortic regurgitation, early enalapril therapy might be beneficial. METHODS: Between 1990 and 1993, 76 asymptomatic nonrheumatic patients with mild to severe chronic aortic regurgitation were enrolled in a randomized, double-blind trial comparing enalapril with hydralazine. All patients underwent serial noninvasive studies. Seventy patients completed the 12-month follow-up. RESULTS: At 1 year, patients receiving enalapril had a significant reduction in left ventricular end-diastolic and end-systolic volume indexes (124 +/- 15 vs. 108 +/- 17 ml/m2, p < 0.01; 50 +/- 12 vs. 40 +/- 14 ml/m2, p < 0.01, respectively) and mass index (131 +/- 16 vs. 113 +/- 19 g/m2, p < 0.01), whereas hydralazine therapy showed no significant changes. Both regimens not only had a significant reduction in left ventricular mean wall stress but also had a mild increase in exercise duration. Only enalapril therapy achieved a significant inhibition of the renin-angiotensin system, in contrast to hydralazine therapy. Moreover, the multiple r2 value from the analysis for end-diastolic volume index using the two variables of age and treatment drugs was 72.1% (p < 0.01). CONCLUSIONS: Both regimens decrease left ventricular mean wall stress. Enalapril therapy achieves significant left ventricular mass regression, left ventricular end-diastolic and end-systolic volume index reduction and renin-angiotensin system suppression. These findings suggest that early unloading enalapril therapy has the potential to favorably influence the natural history of chronic aortic regurgitation.

Aged

Diagnosing and managing unstable angina. Agency for Health Care Policy and Research.

This Quick Reference Guide for Clinicians contains recommendations on the care of patients with unstable angina based on a combination of evidence obtained through extensive literature reviews and consensus among members of an expert panel. Principal conclusions include the following. (1) Many patients suspected of having unstable angina can be discharged home after adequate initial evaluation. (2) Further outpatient evaluation may be scheduled for up to 72 hours after initial presentation for patients with clinical symptoms of unstable angina judged at initial evaluation to be at low risk for complications. (3) Patients with acute ischemic heart disease judged to be at intermediate or high risk of complications should be hospitalized for careful monitoring of their clinical course. (4) Intravenous thrombolytic therapy should not be administered to patients without evidence of ST segment elevation and acute myocardial infarction. (5) Assessment of prognosis by noninvasive testing often aids selection of appropriate therapy. (6) Coronary angiography is appropriate for patients judged to be at high risk for cardiac complications or death based on their clinical course or results of noninvasive testing. (7) Coronary artery bypass surgery should be recommended for almost all patients with left main disease and many patients with three-vessel disease, especially those with left ventricular dysfunction. (8) The discharge care plan should include continued monitoring of symptoms; appropriate drug therapy, including aspirin; risk-factor modification; and counseling.

Ambulatory Care

Amlodipine once a day in stable angina: double-blind crossover comparison with placebo.

Although calcium antagonists form a mainstay of therapy in patients with angina pectoris, the currently available agents have significant limitations. Nifedipine, diltiazem, and verapamil are all high-clearance agents with significant hepatic extraction and rapid clearance, leading to limited and short-lived bioavailability necessitating frequent daily administration. In contrast, amlodipine, a dihydropyridine calcium antagonist, has a long half-life of 35-50 h (compared with 3 to 4 h elimination half-life of diltiazem, verapamil, and nifedipine). After oral doses, the relative bioavailability of amlodipine is high (64%) and absorption is smooth, with peak plasma levels being achieved 6-12 h postdose. Bioavailability is not affected by the consumption of food. In common with other dihydropyridine calcium antagonists, amlodipine is eliminated mainly by metabolism. None of the metabolites of amlodipine has significant calcium antagonist effects in humans. In contrast to verapamil or diltiazem, amlodipine has no effect on sinus or atrioventricular node and little or no effect on the resting heart rate. Amlodipine does not have any appreciable negative inotropic effect with the relevant clinical dose. Other clinical studies have shown amlodipine to be effective when used once-daily in chronic stable angina and vasospastic angina. Comparative studies indicate that the antianginal efficacy of amlodipine is comparable to the beta blocker nadolol and the benzothiazepine calcium antagonist diltiazem. Amlodipine has also been found to provide improved antianginal effects when combined to treatment with beta blockers and/or long-acting nitrates. Treatment with amlodipine either as monotherapy or combined with other antianginal therapy for up to 26 weeks shows that efficacy is maintained, with no evidence of tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

Diagnostic considerations in patients with suspected coronary artery anomalies.

The diagnosis of coronary artery anomalies requires a high index of suspicion during the history and physical examination. Nonspecific presentations are common, although dramatic presentations such as myocardial infarction or aborted sudden death will occur. Typically the results of the physical examination and ECG and the chest x-ray film are normal except with ALCAPA or coronary-artery fistulas. Screening studies such as exercise stress testing have low sensitivity, and a negative evaluation does not rule out the presence of a significant anomaly. These important limitations must be considered. Echocardiography is a practical and frequently diagnostic test if specific attention is paid to the coronary arteries. This examination should be performed in most patients with suspect symptoms. Other noninvasive techniques such as nuclear and cine MRI cardiac imaging may become increasingly important, but their current use is anecdotal. Cardiac catheterization remains the gold standard; however, recognition of important clues and specific angiographic views are required to fully delineate many anomalies.

Adolescent

Quantification of left to right atrial shunts with velocity-encoded cine nuclear magnetic resonance imaging.

OBJECTIVES: The purpose of this study was to evaluate the ability of velocity-encoded nuclear magnetic resonance (NMR) imaging to quantify left to right intracardiac shunts in patients with an atrial septal defect. BACKGROUND: Quantification of intracardiac shunts is clinically important in planning therapy. METHODS: Velocity-encoded NMR imaging was used to quantify stroke flow in the aorta and in the main pulmonary artery in a group of patients who were known to have an increased pulmonary to systemic flow ratio (Qp/Qs). The velocity-encoded NMR flow data were used to calculate Qp/Qs, and these values were compared with measurements of Qp/Qs obtained with oximetric data derived from cardiac catheterization and from stroke volume measurements of the two ventricles by using volumetric data from biphasic spin echo and cine NMR images obtained at end-diastole and end-systole. RESULTS: Two independent observers measured Qp/Qs by using velocity-encoded NMR imaging in 11 patients and found Qp/Qs ranging from 1.4:1 to 3.9:1. These measurements correlated well with both oximetric data (r = 0.91, SEE = 0.35) and ventricular volumetric data (r = 0.94, SEE = 0.30). Interobserver reproducibility for Qp/Qs by velocity-encoded NMR imaging was good (r = 0.97, SEE = 0.20). CONCLUSIONS: Velocity-encoded NMR imaging is an accurate and reproducible method for measuring Qp/Qs in left to right shunts. Because it is completely noninvasive, it can be used to monitor shunt volume over time.

Adolescent

Silent myocardial ischemia in men with systemic hypertension and without clinical evidence of coronary artery disease.

The prevalence, characteristics and circadian pattern of silent myocardial ischemia, and its association with ventricular arrhythmias was studied in hypertensive men aged 35 to 70 years (mean 61) without clinical cardiac disease. Participants were withdrawn from diuretic treatment and received 1 month of oral electrolyte repletion with 40 mmol of potassium chloride, and 400 mg of magnesium oxide daily. Twenty-four-hour Holter monitoring was then performed. Episodes of silent myocardial ischemia occurred in 50 of 186 men (27%) and lasted from 2 to 289 minutes (mean 30 and median 18). Statistical analysis comparing the interval from midnight to 6 A.M. with each of the other three 6-hour time intervals revealed that participants were less likely to have silent myocardial ischemia in this period (p less than 0.01 for each comparison) than at other times of the day. There was little difference in the proportion of men with a frequent or complex ventricular arrhythmia during the entire day or within 1 hour of the silent myocardial ischemic episode (or during a comparable time period) comparing those with to those without silent myocardial ischemia. These findings indicate that silent myocardial ischemia occurs in approximately 25% of an older population of hypertensive men without history of symptomatic cardiac disease. The circadian pattern of frequency of silent ischemic events in men free of clinical cardiac disease is similar to that reported for patients with cardiac disease and coincides with that reported for sudden death. There was no significant association between silent myocardial ischemia and ventricular arrhythmias.

Adult