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 goal of this study was to determine the prevalence and evolution of acquired right ventricular outflow tract obstruction (RVOTO) in the recipient twin in twin-twin transfusion syndrome (TTTS).
Twin-twin transfusion syndrome complicates 4% to 26% of diamniotic monochorionic twin gestations and is associated with high fetal morbidity and mortality. Cardiac dysfunction and biventricular hypertrophy may develop in the recipient twin with the potential for RVOTO.
This was a retrospective review of a two-center experience of TTTS to describe the prevalence and evolution of acquired RVOTO in the recipient twin. Right ventricular outflow tract obstruction was diagnosed or excluded by fetal or postnatal echocardiography or clinical assessment.
Of 73 twin pregnancies with TTTS identified between 1994 to 1998, a total of seven (9.6%) were complicated by RVOTO in the recipient twin: two subvalvar/muscular, four valvar and one combined. Of 44 pregnancies with fetal echo, six had in utero RVOTO with antegrade flow diagnosed at gestational ages ranging from 19 to 27 weeks. In utero progression occurred in four cases over a period of four to eight weeks, with the development of RVOT atresia by delivery. Postnatal progression of RVOTO occurred in two cases, one of which required pulmonary balloon valvuloplasty at age two years. Postnatal regression of subvalvar RVOTO occurred in two cases in early infancy. Death related directly or indirectly to the RVOTO occurred in all four patients who developed complete RVOT obliteration.
Right ventricular outflow tract obstruction may occur in the recipient twin of at least 9% of pregnancies complicated by TTTS. Right ventricular outflow tract obstruction progression is common in utero and may worsen neonatal outcome.
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 aim of the present work was to identify possible associations between individual balances in the activity of the positive and negative reinforcement motivation systems using a method based on emotional modulation of the startle reaction (EMSR) by motivationally significant emotionally positive and negative contextual visual stimuli and measures of cardiovascular system activity. Studies were performed using healthy males (mean age 30.29 +/- 9.8 years) with normal and first-episode excessive increases in arterial blood pressure (systolic blood pressure to greater than 140 mmHg, diastolic to greater than 90 mmHg). Cluster analysis of EMSR data identified groups of individuals with different activity profiles for the positive and negative reinforcement systems. Groups of subjects with changes in the balance of activity towards a lower level of positive reinforcement system activity (smaller startle reflexes to positive contextual stimuli) or a higher level of negative reinforcement system activity (larger startle reactions to threatening contextual stimuli) showed significantly greater baseline SBP and DBP. The possible mechanisms of the modulatory influences of the balance of system activities on autonomic vascular regulatory processes are discussed.