Long-term effects of angiotensin-converting enzyme inhibitors and calcium antagonists on the right and left ventricles in essential hypertension.

To compare the effects of chronic antihypertensive treatment on left and right ventricular structure and function, 24 patients with mild to moderate, never-treated hypertension were randomized to receive fosinopril (20 mg daily) or amlodipine (10 mg daily) for 12 months. At baseline and subsequently at the end of third, sixth, and twelfth months, each patient underwent an integrated echocardiographic study and noninvasive ambulatory blood pressure monitoring. Both drugs significantly reduced blood pressure, casual or monitored (p < 0.01), and left ventricular mass index (from 125 +/- 32 to 100 +/- 12 gm/m2 [p < 0.02] with amlodipine and from 106 +/- 18 to 89 +/- 10 gm/m2 [p < 0.02] with fosinopril). The decrease in left ventricular mass was essentially caused by a reduction of ventricular thickness. Free right ventricular wall thickness was also lowered in both groups, more consistently with amlodipine (from 8.0 +/- 2.1 to 6.4 +/- 0.8 mm; p < 0.01), without an increase in plasma natriuretic peptide and insulin concentrations or heart rate. With both treatments, the decrease in ventricular mass was not associated with impairment of systolic function, whereas a trend toward an improvement of Doppler echocardiographic indexes of biventricular diastolic function was observed. In conclusion, both amlodipine and fosinopril induced similar qualitative effects on anatomy and function of both ventricles. The clinical meaning of these observations must be defined further by means of adequately sized prospective trials.

Prolonged streptokinase infusion in patients with unstable angina: results of a randomized, placebo-controlled clinical trial.

BACKGROUND: The purpose of this study was to assess the efficacy both of prolonged (48 h) and of short-duration (1 h) administrations of streptokinase in patients with unstable angina. In unstable angina, thrombosis is a dynamic process that waxes and wanes for hours and even days. The majority of previous studies have investigated the efficacy of short-duration thrombolytic regimens. METHODS: One hundred patients with acute unstable angina were randomly allocated to receive placebo, 1,500,000 U streptokinase during 1 h or 250,000 U streptokinase during 1 h and then a prolonged infusion of 100,000 U for the next 48 h. All of the treatments included intravenous heparin administration for 72 h. RESULTS: No death occurred in the study population. One of 34 patients treated with placebo (2.9%), three of 33 treated with streptokinase during 1 h (9.0%) and three of 33 treated with streptokinase during 48 h (9.0%) had a myocardial infarction. Refractory angina occurred in nine, three and seven patients receiving placebo, streptokinase during 1 h and streptokinase during 48 h, respectively. Kaplan-Meier analysis showed that the total probability for a patient to be free of cumulative events did not differ among the three groups of patients (NS). Fourteen patients (41%) receiving placebo, 15 patients (45%) receiving streptokinase during 1 h and 14 patients (42%) receiving streptokinase during 48 h had ischaemic episodes detected by Holter monitoring during the first 72 h after hospital admission (NS). Two patients receiving streptokinase during 48 h required blood transfusion, and a greater incidence of minor bleeding (P < 0.05) and adverse events (P < 0.02) was observed in patients receiving prolonged streptokinase administration than in those receiving streptokinase during 1 h or placebo. CONCLUSIONS: In patients with acute unstable angina, the administration of two different regimens of streptokinase significantly reduces the probability neither of developing cardiac events during hospitalization nor of ischaemia detected by Holter monitoring in the early phase after hospital admission. Although the sample size of the study provided sufficient power to exclude only a large difference in effect size, it did allow us to detect a significantly higher incidence of bleeding in the group of patients treated with prolonged streptokinase infusion.

Early predictors of smoking cessation after myocardial infarction.

The determinants of long-term smoking cessation were evaluated in 80 patients who smoked cigarettes and survived a myocardial infarction. All patients underwent a program of rehabilitation and secondary prevention including in-hospital counseling and physician-guided reinforcing sessions at 1, 3, and 6 months after discharge. At 18 months of follow-up, 53 patients (66.3%) had quit smoking. Variables associated with smoking cessation were duration of hospital stay greater than or equal to 19 days (79 vs. 48%; p less than 0.005) and peak creatine phosphokinase (CPK) elevation greater than or equal to 500 U/l (76 vs. 54%; p less than 0.05). Males tended to quit in higher proportion than females (68 vs. 44%). Age, prior myocardial infarction, other cardiovascular risk factors, infarction location, Killip class at entry, and duration of stay in coronary care unit did not significantly affect the quitting rates. Logistic regression analysis singled out the duration of hospital stay as a significant predictor of smoking cessation (p less than 0.005). Early and intensive secondary prevention during the hospital stay is crucial in promoting sustained smoking cessation after myocardial infarction.

[Analysis of clinical history and predictive factors in the prognosis of a group of young patients with acute myocardial infarct]. / Analisi della storia clinica e fattori predittivi della prognosi in un gruppo di pazienti giovani con infarto miocardico acuto.

A retrospective study was carried out to examine the clinical history and coronarographic and ventriculographic aspects of a young group of patients aged under 40 affected by acute myocardial infarction. The study confirmed previously published findings with regard to the low rate of mortality, both in hospital and shortly after necrosis. On the other hand, non-fatal ischemic attacks were common in this population and were significantly correlated to the extension of coronary disease. Ischemic complications in this group of patients were mainly treated using coronary revascularisation (by-pass or PTCA), procedures which have been proved efficacious in preventing further ischemic events during the medium term. The results of the study indicate the need for a more aggressive approach, with the use of predischarge coronarography even in the absence of residual ischemia. This would not only serve to ascertain the degree of coronary disease or revascularisation, but above all would enable a prognosis to be given regarding the patient who, in psychological terms, should not be considered an invalid following acute ischemia.

[Left ventricular hypertrophy in hypertension: functional aspects]. / L'ipertrofia ventricolare sinistra nell'ipertensione: aspetti funzionali.

The purpose of this study was to detect the anatomical and functional response of the left ventricle in essential, uncomplicated hypertension. Fifty outpatients, whose hypertension (DBP greater than 95 mmHg on three separate visits) had been documented from few weeks to a maximum of 5 years, showing neither electrocardiographic abnormalities nor other signs referable to target organ damage, underwent an M-mode, computerised echocardiographic study. Twenty-seven patients has never been treated, and 23 patients were withdrawn from previous treatments for at least one month. Echocardiographic data of the left ventricle were compared with those of 38 normals, matched by sex, age and body surface area. Hypertensives showed a significant increase in both LV mass index (p less than 0.001) and relative wall thickness (p less than 0.001), a pattern of concentric hypertrophy, which prevented an inappropriate rise in wall tension. Twenty-four patients, whose LV mass was above the mean normal value plus two standard deviations, were considered to have left ventricular hypertrophy. The remaining 26 patients were classified as non hypertrophic, for their mass resulted lower than the mean value of controls plus 2 SD: left ventricular mass was 152 +/- 32 g/m2 and 97 +/- 19 g/m2, respectively (p less than 0.001). Systolic performance was enhanced in both subgroups of hypertensives, since their values of fractional shortening and those of mean-Vcf were both above the line which represents the normal relationship with end-systolic stress. Diastolic relaxation, evaluated by means of time to peak filling rate, was impaired only in the hypertensive subjects with increased LV mass (p less than 0.001 vs. normotensive), being retained in the non-hypertrophic patients. In the whole hypertensive group, LV mass index poorly correlated with casual systolic blood pressure (r = 0.31; p less than 0.05), while time to peak filling rate showed a good correlation with LV mass index (r = 0.76; p less than 0.001). We conclude that: 1) in essential hypertension without electrocardiographic abnormalities or target organ damage, echocardiographic left ventricular hypertrophy is a rather frequent finding; 2) the pattern of concentric hypertrophy, by reducing the increase in wall tension due to pressure load, contributes to the retained, or enhanced, systolic performance seen in our series; 3) on the other hand, left ventricular filling seems to be impaired in relation to the degree of myocardial hypertrophy.

Left ventricular mass and function before and after antihypertensive treatment.

We have studied the effect of blood pressure control upon left ventricular mass and function. Twenty hypertensive patients without clinical or electrocardiographic signs of cardiac involvement were given sequentially: placebo for two weeks; captopril (250 mg/day) for eight weeks; and captopril (125 mg/day), alone or combined with chlorthalidone (25 mg/day), for eight weeks. M-mode echocardiography was performed at the end of placebo period, after eight and after 16 weeks active treatment. Blood pressure was significantly reduced (p less than 0.01) by therapy, the maximum decrease being observed at the end of the study. Similarly, interventricular septal thickness, posterior wall thickness and left ventricular mass index showed a significant reduction (P less than 0.01 at the eighth and P less than 0.001 at the 16th week), while no changes were detected in left ventricular function. Furthermore, both wall stress index at end-diastole and end-systolic stress were significantly lowered by treatment (at the 16th week P less than 0.01 and P less than 0.001, respectively). Baseline systolic blood pressure was inversely correlated with the ratio of the left ventricular radius to posterior wall thickness (r = -0.97, P less than 0.001) but no relation was found between post-treatment fall in either systolic or diastolic blood pressure and left ventricular mass index. After treatment more patients showed normal left ventricular wall thickness in relation to systolic blood pressure. We conclude that in uncomplicated hypertensive patients captopril, either alone or combined with chlorthalidone, can reverse left ventricular hypertrophy by decreasing both septal and posterior wall thickness.(ABSTRACT TRUNCATED AT 250 WORDS)