Esther Henderson

Ventricular Arrhythmias in Patients with Hypertensive Left Ventricular Hypertrophy

In patients with hypertension, a pattern of left ventricular hypertrophy on the electrocardiogram is associated with a risk of sudden death in excess of the risk attributable to hypertension alone. We therefore investigated the frequency of complex ventricular arrhythmias by means of 48-hour ambulatory electrocardiographic monitoring in 100 treated hypertensive patients, of whom 50 had electrocardiographic evidence of left ventricular hypertrophy and 50 did not, and in 50 normotensive controls. The groups were matched for age, sex, and smoking habits, and the two hypertensive groups were matched for blood-pressure levels before and after antihypertensive therapy. Nonsustained ventricular tachycardia, defined as greater than or equal to 3 complexes at a rate greater than or equal to 120 beats per minute, occurred in 14 (28 percent) of the 50 patients with an electrocardiographic pattern of left ventricular hypertrophy, in 4 (8 percent) of the 50 patients without hypertrophy (P less than 0.05), and in 1 (2 percent) of the control subjects. Eight of the 50 patients (16 percent) with hypertrophy had episodes of nonsustained ventricular tachycardia longer than 5 complexes, whereas no patients without hypertrophy and no controls had such episodes. The group with nonsustained ventricular tachycardia was characterized by a high left ventricular mass on echocardiography and a high prevalence of ST-T abnormalities on electrocardiography. Ventricular tachycardia was not closely related to blood-pressure levels, nor was it associated with diuretic therapy or hypokalemia. The clinical importance of these arrhythmias is uncertain. Nevertheless, our data suggest that complex ventricular arrhythmias occur commonly in hypertensive patients with left ventricular hypertrophy and may contribute to the higher incidence of sudden death in these patients.

Non-invasive determination of cardiac output by Doppler echocardiography and electrical bioimpedance.

Cardiac output measured by thermodilution in 25 patients within 24 hours of acute myocardial infarction was compared with cardiac output measured by Doppler echocardiography (24 patients) and electrical bioimpedance (25 patients). The mean (range) cardiac outputs measured by Doppler (4.03 (2.2-6.0) 1/min) and electrical bioimpedance (3.79 (1.1-6.2) 1/min) were similar to the mean thermodilution value (3.95 (2.1-6.2) 1/min). Both non-invasive techniques agreed closely with thermodilution in most patients. None the less, three results with each method disagreed with thermodilution by more than 1 1/min. Both non-invasive techniques were reproducible and accurate in most patients with acute myocardial infarction. Doppler echocardiography was time consuming and technically demanding. Electrical bioimpedance was simple to use and had the additional advantage of allowing continuous monitoring of the cardiac output.

Effect of captopril, an angiotensin-converting enzyme inhibitor, in patients with angina pectoris and heart failure.

The effects of captopril and placebo were compared in 18 patients with chronic heart failure and angina pectoris with use of a double-blind crossover trial design. Symptoms were assessed by patient treatment preference, visual analogue scores and nitroglycerin consumption. Exercise performance was assessed using two different treadmill protocols of different work intensity with simultaneous measurement of oxygen consumption and by supine bicycle exercise and simultaneous radionuclide ventriculography. Arrhythmias were assessed by 48 h ambulatory electrocardiographic monitoring. Patients generally preferred placebo to captopril, and this appeared to be due to an increase in symptoms of angina with captopril. Treadmill exercise time on a high intensity protocol was shorter with captopril than with placebo; on a low intensity protocol, angina became a more frequent limiting symptom even though overall exercise performance was not changed. The heart rate-blood pressure product was reduced, but largely because of a reduction in blood pressure rather than in heart rate. During supine bicycle exercise, no differences in symptoms, exercise performance, ejection fraction or changes in blood pressure were noted and ventricular arrhythmias were reduced. Captopril does not appear to be clinically useful in alleviating angina pectoris in patients with heart failure, and this effect may be related to a decrease in coronary perfusion pressure. Nonetheless, desirable metabolic effects, a reduction in arrhythmias and potential effects on survival require further study of captopril in patients with both angina and heart failure.

Increased circulating atrial natriuretic factor concentrations in patients with chronic heart failure after inhibition of neutral endopeptidase: effects on diastolic function

Objective—±Candoxatrilat was used to raise atrial natriuretic factor (ANF) concentrations in patients with heart failure, and the effects on left ventricular systolic and diastolic function were studied to determine the contribution of peripheral and central mechanisms to the haemodynamic effects. Design—This was a single blind, randomised comparison of ±candoxatrilat and placebo in patients with mild heart failure. All patients received two intravenous doses of ±candoxatrilat and two placebo doses on four consecutive days. Setting—A teaching hospital department of cardiology. Patients—Six men (mean age 52 years) with mild heart failure (New York Heart Association class II) due to ischaemic heart disease (four patients) or dilated cardiomyopathy (two patients) were included. Mean ejection fraction was 37·5% and mean peak oxygen consumption was 20·4 ml/min/kg. Main outcome measures—Plasma ANF concentrations, haemodynamic indices and left ventricular diastolic function measured by early to atrial filling rate (E:A ratio) with Doppler echocardiography were determined before and after ±candoxatrilat and placebo. Results—±Candoxatrilat caused a threefold rise of plasma ANF compared with placebo (p < 0·005), but there was no significant change in heart rate, blood pressure, or cardiac output. Mean right atrial pressure fell from 6·7 to 4·7 mm Hg (NS) and pulmonary artery wedge pressure fell from 9·2 to 6·7 mm Hg (p < 0·05). Doppler echocardiographic measurements of transmitral blood flow showed a significant fall in peak early left ventricular filling velocity from 39·5 to 34·2 cm/s (p < 0·05), along with a non-significant rise in peak atrial filling velocity from 39·7–41·6 cm/s after ±candoxatrilat. The E:A ratio, a Doppler index of left ventricular diastolic function, fell from a mean of 1·04 to 0·87 (p < 0·05). Conclusions—±Candoxatrilat increased plasma ANF concentrations and reduced right atrial and pulmonary artery wedge pressures. No evidence of an improvement in left ventricular systolic or diastolic function was found, so the fall in preload was due to peripheral effects, either an increase in venous capacitance or a fall in circulating blood volume.

Atenolol and celiprolol for stable angina pectoris

Once-daily atenolol and celiprolol were compared in a placebo-controlled crossover study of 16 patients with stable angina pectoris. Atenolol and celiprolol equally and significantly reduced frequency of angina and electrocardiographic evidence of cardiac ischemia. Celiprolol, however, produced less suppression of the double product at 1 mm of ST-segment depression than atenolol, suggesting that actions other than reduction of heart rate may contribute to its antianginal efficacy.

Acute effects of cicletanine in angina pectoris.

SummaryThe anti-anginal properties of single doses of a new anti-hypertensive drug, cicletanine, were investigated in a double-blind, randomised, balanced, crossover comparison with placebo in sixteen patients with chronic stable angina pectoris.All subjects underwent treadmill exercise 2 h after drug administration and 24 h ambulatory ECG monitoring with ST scanning. Although there were significantly fewer episodes of ST depression on ambulatory monitoring after cicletanine, total exercise duration and time to 1 mm ST depression were unchanged.This report provides little evidence of an acute anti-anginal effect of cicletanine but longer term studies may be indicated to further evaluate this drugs potential role in the management of angina pectoris.