Evaluation at patients with ventricular arrhythmias and coronary artery disease of myocardial revascularization effects.

UNLABELLED: The aim of this study was to determine the relations between myocardial revascularization therapy--coronary artery bypass graft (CABG) and coronary angioplasty (PTCA)--and ventricular potentially malignant arrhythmia (VPMA) (coupled VPC, VPC > 10/hour, NSVT--Morganroth classification), in patients (pts) with stable CAD. METHODS: 765 patients with stable angina and ventricular potentially malignant arrhythmia were evaluated angiochoronarographically, echographically, by programmed electrical stimulation (PES), standard ECG, Holter ECG, radiologically, and by stress test. From 765 patients with CAD and VPMA 169 pts. (22.9% of cases) were revascularized, 77 pts. (10.06% of cases) by CABG surgery and 82 pts. (10.71% of cases) by PTCA with or without stenting. RESULTS: From pts. with inducible sustained ventricular tachycardia by programmed electrical stimulation PES + (129 pts. 16.86% of cases), 19 pts. (2.5% of cases) were with CABG vs 9 pts. (1.17% of cases) with PTCA (p > 0.05). In 333 pts. with arrhythmogenic myocardic ischemia detected by Holter ECG/24 hours (Holter +) the distribution of myocardial revascularization was similar (40 pts., 5.22% of cases with CABG vs 46 pts., 6.01% of cases with PTCA) (p > 0.05). The study included 225 pts. with positive stress test, 45 pts. were revascularized, 18 pts. (2.35% of cases) with CABG and 27 pts. (3.52% of cases) with PTCA (p > 0.05). Revascularized pts. represent an increased percent with prior myocardial infarction in the subgroup with CABG vs. PTCA (39% of cases, p < 0.05 vs. 25% of cases, p < 0.05). Revascularized pts. presented similar distributions of VPMA in subgroups with CABG and PTCA. CONCLUSIONS: VPMA was not influenced by myocardial revascularization, CABG or PTCA, the incidence being similar (50.94% vs 47.2%; p < 0.05) with pts. drug treated.

Pathophysiology of coronary artery in-stent restenosis.

In-stent restenosis reflects the interaction of a cascade of molecular and cellular events occurring within the vessel wall. Coronary stenting induces localized injury to the vessel wall, which leads to the release of thrombogenic, vasoactive, and lymphocytes mitogenic factors that result in processes causing re-narrowing at the injured site. Three major processes have been identified that lead to the in-stent restenosis: neointimal hyperplasia, elastic recoil, and negative arterial remodeling. The most important one is intimal hyperplasia. As the time course of neointimal hyperplasia is unknown, a causal relationship between the development of new blood vessels and clinical restenosis cannot be firmly established.

The cardiac insufficiency talinolol study (CITAS) study design.

Beta-blockers without partial agonist activity are now considered to be strategic therapy for patients with chronic heart failure, but many issues remain to be clarified. The objective of the double-blind, randomized, placebo-controlled cardiac insufficiency talinolol study (CITAS) is to assess efficacy and safety of talinolol - a selective beta-1 adrenoreceptor blocker - in patients with ischemic and non-ischemic heart failure. The primary end-point refers to the influence of talinolol on exercise capacity, evaluated by 6-min walking-test. Secondary end-points consist of left ventricular function, cardiovascular and all-cause mortality, hospitalizations, quality of life, combined clinical end-points and adverse events. There were enrolled 294 patients with stable heart failure in NYHA class II-IV, LVEF <40%, receiving diuretics, ACE-inhibitors and optionally nitrates and digoxin. Talinolol was titrated up to 100 mg/day (one arm) or to 150 mg/d (the other arm), starting with 12.5 mg daily. Enrollment began in November 1997 and the last visit will be in December 2000.

Ethyl alcohol and dilative cardiomyopathy.

The ethanol-induced dilative cardiomyopathy has a complex clinical and paraclinical picture because of the direct action of the alcohol and the indirect action of its metabolites on human myocardium and neuroendocrine system. Ventricular arrhythmias, atrial arrhythmias, and heart failure are significant and show a great sensitivity of the conduction system. Working myocardium is also affected, which is proved by the impaired systolic and diastolic function of the heart and by the nitroglycerine-resistant isovolumetric relaxation time.

[The effects of nitroglycerin administered intravenously in acute myocardial ischemia]. / Efectele nitroglicerinei administrata intravenos în ischemia miocardica acuta.

The effects of i.v. nitroglycerin were studied by ECG and enzymatically in 16 patients (mean age 57.9 +/- 1.4 years) (NTG) in comparison with a control lot (c) of 17 patients (mean age 62.7 +/- 2.1 years) treated with dipyridamole and/or nifedipine (N), admitted in the first 4-10 hours after the onset of the first symptoms. The patients with heart failure and those with Q waves and CPK or LDH values greater than 2 x n were not admitted. NTG was administered in doses of 20 micrograms--60 microgram/hour for 24-96 hours and systolic AT (s) was kept under 10% of the basic values but not under 100 mmHg. Myocardial infarction appeared in 9 N-treated patients (54.86%) and 11 controls (58.25%) (p = 0.07). The size of myocardial necrosis was reduced in the N-treated patients. Peak serum CPK levels had considerably less increases in N (from 72.9 U to 73.4 U) (p greater than 00.5) versus C from 34.2 U to 364.5 U) (p less than 0.001). The sum of segmentary depression failed from 9.13 mm to 3.19 mm (p less than 0.05) in N, whereas in C the decrease was not significant (6.12 mm as against 9.38 mm; p greater than 0.05). The evolution was severe in C, as the angina crises (14 cases versus 2 cases, p less than 0.01) and the extension of the infarction (8 cases versus, 0; p 0.05) less than 0.05) appeared more frequently than in N. Only two patients in C died (p less than 0.05). Therefore, i.v. NTG administration in small doses in acute myocardial infarction leads to immediate disappearance of the anginal pain, lowers the extent of the myocardial necrosis and improves the clinical evolution.

Effects of verapamil on the acute experimental myocardial ischemia.

The hemodynamic effects of verapamil in conditions of myocardial ischemia and its influence on the atrio-ventricular conduction were investigated in 13 dogs with transient repeated occlusions of the anterior descending coronary artery. Verapamil 0.25 mg/kg was administered after control determinations of heart rate, LV dp/dt, systolic and diastolic arterial pressure and the mean sum of S--T segment elevations recorded by means of 9 epicardial electrodes. Comparison of the differences between the control data and those after occlusion, on the one hand, and those before and after occlusion + verapamil, on the other hand, showed that the drug did not induce significant hemodynamic changes. Arterial pressure was slightly lowered; the increase of LV dp/dt noted after occlusion without verapamil did not occur any more and the S-T segment and T wave disturbances were also less marked, suggesting a protective effect on the ischemic lesion. Larger doses of verapamil (0.50-0.75 mg/kg) induced second and third degree A-V blocks in three animals. These effects could be controlled in two animals by previous or subsequent administration of Carbocromen.

Prognostic value of postextrasystolic potentiation in patients with acute myocardial infarction.

To assess the functional reserve of left ventricle and appreciate prognosis in patients with acute myocardial infarction (AMI) showing ventricular premature beats, the systolic time intervals (STI) and the apexcardiogram (ACG) were determined in sinus rhythm and at the first postextrasystolic beat in 30 patients with AMI (12 mens, 18 women, average age 49 years), distributed into the first three functional classes (Killip), 10 in each class. Location of AMI was anterior in 21 cases, inferior in 1 and anteroinferior in 8. At the first postextrasystolic beat, class III patients showed a lengthening of PEP interval and increase of the PEP/LVET ratio, compared to those in initial sinus rhythm, thus indicating an absence of potentiation; ACG tracings in the same group revealed a lengthening of isovolumic relaxation time (IRT). In classes I and II, both the STI measurement and ACG data indicated the presence of potentiation at the first postextrasystolic beat, manifested by PEP shortening and decrease of PEP/LVET ratio, as well as by a reduction of IRT. Of the patients in classes I and II, only one developed heart failure, while of class III patients, 4 died of heart failure within one year and 3 showed cardiogenic shock on admission. The absence of potentiation in the latter category (with congestive heart failure) is interpreted as a sign of severe prognosis for the subsequent course and outcome of AMI.