BACKGROUND: Left ventricular hypertrophy is frequently noted in patients with moderate to severe chronic renal failure not requiring dialysis. Recently, several studies have shown reversal of myocardial hypertrophy in end-stage renal disease with long-term pharmacological control of blood pressure, but it is unclear whether left ventricular mass regresses or normalizes with antihypertensive treatment of patients with earlier stages of chronic renal failure. METHODS: Seventy-two undialysed patients with chronic renal failure, chronic mild-to-moderate hypertension, and left ventricular hypertrophy were randomly assigned in a prospective study to either the captopril (n = 36) or enalapril group (n = 36). Blood pressure measurements, echocardiographic and Doppler parameters were evaluated before treatment and at 6 and 12 months of therapy. RESULTS: During follow-up, six patients developed side-effects including dry cough, taste disturbances, skin rash and gastric intolerance. In the captopril group there was a decrease in mean left ventricular mass index by 12% after 6 months of treatment, which decreased by 20% after 12 months treatment. For enalapril, the average reduction of myocardial mass after 6 months treatment was 14% and after 12 months treatment, the decrease was 19%. In both treatment groups there was significant improvement of left ventricular filling dynamics. No deterioration of left ventricular systolic function was observed. CONCLUSIONS: Our results confirm that antihypertensive monotherapy with the ACE inhibitors, captopril and enalapril, in patients with chronic renal failure results in regression of left ventricular mass index associated with a significant improvement in the diastolic function of the left ventricle without a demonstrable deterioration in left ventricular systolic performance.
The hemodynamic and metabolic effects of acetate were studied in rats in vivo and in the isolated perfused heart. Hemodynamic parameters, myocardial phosphagens, inorganic phosphate, and adenosine were measured in vivo. Acetate uptake, coronary flow, O2 consumption, parameters of the cellular energy state, and hypoxanthine compounds and their washout were measured in heart perfusion experiments. Heart rate (HR), cardiac output, and the peak derivative of the left ventricular pressure rise (dP/dtmax) increased significantly during acetate infusion in vivo, but mean arterial pressure, systolic arterial pressure, and systemic vascular resistance decreased. Heart muscle ATP concentrations decreased after 7 min of acetate infusion. In vivo cardiac work load (HR.(peak left ventricular pressure] showed a positive correlation with tissue adenosine concentration and a negative correlation with phosphorylation potential. Acetate uptake in the perfused hearts was about 2.5 mumol/min per gram wet weight. Acetate perfusion increased O2 consumption and coronary flow concomitantly with a decrease in tissue ATP concentration. Tissue AMP and perfusate effluent adenosine concentration and adenosine output increased significantly, perfusate adenosine showing a non-linear positive correlation with coronary flow. The results demonstrate that acetate induces considerable changes in hemodynamics and metabolism in the heart.
Overall fifty one patients with chronic cardiac insufficiency (ChCI) were studied for changes in parameters characterizing hemodynamics and lipid peroxidation (LPO) under treatment with kapoten and prazosin. Kapoten was found to be capable of exerting an antioxidant effect and working in ways beneficial for the pulmonary circulation, while prazosin is generally indicated to patients with ChCI presenting with increased end diastolic pressure in the left ventricle. Prazosin activates LPO, for which reason its pro-oxidant action needs to be drug-corrected. Because of marked pharmacologic effects of both drugs in dealing with refractory circulatory insufficiency it is advisable that further studies be made in order that we might be able to determine indications for kapoten and prazosin therapy in coronary patients as well as those with arterial hypertension, cardiomyopathies, valvular defects, ChCI with complications more accurately.
The authors examined 68 patients aged from 42 to 68 years with ischemic heart disease without a history of myocardial infarction and with angina pectoris of exertion functional class 2-3 and circulatory insufficiency class 2 (according to NYHA criteria). The criteria serving as the reason for relating patients to the follow-up group were left-ventricular end-diastolic volume > 160 ml, ejection fraction 0.55, threshold power of endured loads within a range of 71.5 +/- 2.30 watt. After stabilization of the clinical status by means of basic therapy (nitrates, blockers of slow calcium channels, diuretics, antiaggregants), all patients were divided into two follow-up groups. The first group consisted of 36 patients who received renitec (10 mg/24 h), patients of group 2 were given enap in the same dose. The course of treatment lasted 12 weeks. The effectiveness of treatment was controlled by echocardiography according to the standard methods in M- and B-regimens. Analysis of the obtained data showed that within 12-day follow-up renitec demonstrated higher effectiveness and lesser incidence of side-effects than did enap given in the same dose.
The noninvasive method of oscillovasometry, devised previously, was applied to the estimation of arterial pressure, effective radius of large arterial vessels, a number of indices showing elastic vessel properties and change in tone of the vessels on the right upper limb just before sublingual administration of nitroglycerin (0.5 mg) to the patients and 4-5 min after it. A group of 96 patients with different levels of arterial pressure were examined. It was found that all the patients showed a pressure decrease and tachycardia, but about a half of them had a passive response in large arterial vessels in the form of a decrease in the vessel volume, while others showed a decrease in arterial vessel tone (vasodilation), i.e. an active vascular response. From the data we drew the conclusion that there are two types of vascular response (active and passive) and they do not depend on the initial level of arterial pressure. Nitroglycerin probably acts more effectively on large arteries with a high initial tone. The possible mechanism of this phenomenon is discussed.
The acute effects of ethanol (1.0 g/kg and 1.5 g/kg, n = 4 and n = 5, yielding blood concentrations of 1.3 +/- 0.2 mg/ml and 2.4 +/- 0.3 mg/ml) on myocardial perfusion were studied in anesthetized, thoracotomized, artificially ventilated dogs by using a radioactive microsphere technique. The control group (n = 5) received saline. The smaller dose of ethanol decreased perfusion in the left ventricular myocardium from 0.737 +/- 0.122 to 0.555 +/- 0.122 ml/g/min (NS), whereas the greater dose nonsignificantly increased it, from 0.744 +/- 0.115 to 0.819 +/- 0.119 ml/g/min (p
The short- and long-term hemodynamic effects of encainide, a new class IC antiarrhythmic agent, were studied in 25 patients (mean age 61 +/- 11) with complex symptomatic ventricular arrhythmia and left ventricular dysfunction. Ninety-two percent had previous myocardial infarction and 8% had dilated cardiomyopathy. Seventy-five percent had congestive heart failure, class III or IV, according to the New York Heart Association. All patients underwent a nuclear ventriculogram performed at least 3 days after discontinuing previous antiarrhythmic drugs. Nuclear ventriculograms were repeated 1 to 6 weeks later while the patients were receiving therapeutic doses of encainide ranging from 75 to 300 [corrected] mg/day. Nuclear ventriculograms were also repeated after 6 months or 1 year of encainide therapy in 16 of these patients. Encainide did not have significant effects on heart rate, blood pressure, left ventricular ejection fraction, systolic or end-diastolic volumes. None of the patients showed a worsening of congestive heart failure during encainide therapy. These results compare favorably with those of other class I antiarrhythmic agents. A review of published reports on the hemodynamic effects of intravenous encainide shows it to have a mild but statistically significant dose-related depressant effect on cardiac function. This effect, however, appears to be no different from that of other newer class I agents.