Ventricular late potentials in acute myocardial infarct

Ventricular late potentials are regarded as an expression of delayed impulse conduction in an area of myocardial ischemia and, accordingly, indicative of a preformed reentry circuit. Late potentials can be detected in chronic, stable coronary artery disease and their presence correlates closely with impairment of ventricular function and with the probability of future occurrence of tachyarrhythmic events or sudden cardiac death. While repetitive ventricular arrhythmias in the chronic stage of coronary artery disease result almost invariably from circling intraventricular wavefronts, tachyarrhythmias associated with acute myocardial infarction appear attributable to differing pathomechanisms. According to experimental studies, in acute myocardial infarction, three phases of arrhythmogenesis can be differentiated: phase 1 encompasses the first hours after vessel occlusion which generally corresponds with the prehospital phase. Due to the difference in potential of up to 25 mV between ischemic and nonischemic cardiac muscle areas, an injury current is called into existence which leads to depolarization of normal cardiac muscle tissue. The ectopic impulses so precipitated, the conduction of which is supported by the functional inhomogeneity of the infarcted region, are capable of initiating reentry tachycardia. During phase 2, a few hours to days after the ischemic event, only the subendocardial Purkinje fibers in the infarcted region exhibit focal arrhythmogenicity. In contrast to the working myocardial cells, the latter survive due to their immediate proximity to the cardiac chamber and show, ischemia-induced, a propensity to high-frequency impulse formation in terms of abnormal automaticity. Similar to the experimental findings, the cause of the frequently-observed ventricular arrhythmias in the early hospital phase appears predominantly attributable to a focal arrhythmia mechanism. During phase 3, several days to weeks after the acute myocardial ischemic event, reentry mechanisms again are in the foreground in which the electrophysiologic changes in the Purkinje fibers, in terms of increasing desynchronization, together with conduction barriers arising through the infarct scar, pave the way for reentry phenomenon. After abrupt restoration of patency of a previously occluded vessel the very frequent "reperfusion arrhythmias" are also attributable primarily to reentry mechanisms due to inhomogeneous improvement of the conduction properties in the region of the reperfused myocardium. Ventricular late potentials can be registered both invasively by means of epi- or endocardial leads as well as noninvasively from the body surface.(ABSTRACT TRUNCATED AT 400 WORDS)     

Rupture of the heart in the acute phase of myocardial infarct. Anatomic-macroscopic study]

The data of the macroscopical-anatomical examination of 14 cases of cardiac rupture (10 women, 4 men) complicating acute myocardial infarction were compared with those obtained at autopsy, with the same protocol, in 31 cases of myocardial infarction which resulted in death before the 30th day after the onset. Many anatomical facts separated both groups from each other (size, aspect, limits of myocardial necrosis, state of the coronary arteries). Eventual surgical conclusions might be drawn from this study.     

Surgical revascularization in acute myocardial infarct]

To determine the potential role of emergency surgical revascularization as treatment of acute myocardial infarction (AMI), results in 79 patients undergoing operation for myocardial revascularization during AMI from January 1986 to January 1991 were reviewed. Clinical characteristics for inclusion in the study were: 1) emergency operation; 2) persistent angina not controlled by medical therapy; 3) fixed ST segment elevation until surgical procedure, independently from magnitude of enzymatic levels. The 79 patients were divided in 2 groups: 27 with AMI or evolving AMI (Group 1); 52 with AMI due to complications during PTCA (Group 2). Twenty-eight patients had extremely severe clinical conditions. Mean interval between the beginning of AMI and operation was 4.2 +/- 6.7 hours, with a statistically significant difference between Group 1 (8.7 +/- 10.0) and Group 2 (1.9 +/- 1.0). One hundred ninety-two grafts were performed (2.4 +/- 1.1 grafts/patient). Overall hospital mortality was 10.1% (CL 6.7-13.3) (8 deaths) with a difference between Group 1 [18.5% (CL 10.7-25.3)] and Group 2 [5.8% (CL 4.7-6.6)] (p = 0.074). The incidence of perioperative myocardial infarction was 30.4% (CL 24.9-35.1) for that one in the area of ischemic muscle and 2.6% (CL 0.8-4.1) for infarction in remote muscle. Multivariate analysis for the entire series (79 patients) identified as independent predictors of increased in-hospital mortality: preoperative cardiogenic shock (p = 1.000E-4) and hyperlipidemia (p = 0.008). In Group 1 multivariate analysis identified as independent predictors of increased in-hospital mortality: the attempt of revascularization by PTCA and hyperlipidemia; in Group 2: preoperative need of mechanical ventilatory support.(ABSTRACT TRUNCATED AT 250 WORDS)     

长程晚电位影响心肌缺血再灌注心电稳定性的临床研究

目的　探讨急性心肌梗死 (AMI)病人梗死相关动脉 (IRA)再通对晚电位 (VLP)的动态影响。方法　AMI患者 3 8例 ,于溶栓开始前佩戴数字化Holter记录仪进行 2 4h的长程晚电位连续监测 ,然后将病人分设两个亚组 :溶栓成功组与溶栓不成功组 ,比较这两组病人在溶栓前后VLP各项参数的变化情况 ,找出其与冠脉再通情况之间的关系。结果　AMI患者在溶栓前和溶栓后 3 0min内 ,VLP各项参数无明显统计学差异 ,而溶栓 2～ 3h后 ,再灌注组VLP各参数的数值明显变化 ,而无再灌注组则无这种变化。结论　再灌注在迅速恢复心肌缺血的情况下 ,于溶栓后早期可显著降低VLP的发生率 ,这不仅为临床提供了又一种新的评价冠脉再通的无创检测方法 ,且纠正了传统认为的VLP只有在心肌纤维瘢痕的基础上才能形成的认识     

Hemodynamic variants of acute myocardial infarct]

In 165 patients with myocardial infarction admitted to the clinic within the first 24 hours of the disease the size of the zone of the lesion and its dynamics were appraised in the immediate 4-5 days. Cartographic ECG analysis and study of the vectorcardiogram in dynamics and analysis of the creatine phosphokinase activity curves make it possible to appraise the dynamics of the necrotic zone in the first days of myocardial infarction. It was found that in most patients with macrofocal myocardial infarction the zone of the necrosis increases both in length and in depth in the first days of the disease.     

Pulmonary complications of acute myocardial infarct. Therapeutic orientation]

The heart and the lung make up an inseparable anatomic and functional unit. The changes in one affect the other and vice versa. In acute myocardial infarction a heart failure syndrome develops. This syndrome is characterized by passive pulmonary congestion, which leads to hypoxemia. This hypoxemia indicate the functional disturbance of the lung, and the hemodinamic evolution of the disease. Arterial gases determination is the best way to assess the sickness progression. A certain paralelism exists among the central venous saturation, cardiac insufficiency and the degree of pulmonary disfunction. Such a procedure is not very appreciable and does not substitute the direct analysis of the arterial PO2. The pulmonary complications in the myocardial infarction shock are directly responsable of death in 50% of the patients. To heart failure and shock, hipperfusion and hypoxia are added. Many vessels close due to the decrease in the pulmonary flow. This brings about the release of substances that are toxic to the vessel causing an inflammatory vascular reaction. The decrease in the flow harms the lung cell and for this reason atelectasia or alveolar colapse occur; besides inducing the formation of shunts. Under these conditions the lung compliance decreases. The areas that are badly ventilated and hypoperfused can easily become infected and pneumonitis and abscesses cause even more harm to the tissue. The decrease in the speed of circulation and hematologic changes of shock, induce a diseminated intravascular coagulation. What was stated before leads to an important reduction of the lung as a depurating organ and makes the shock irreversible. As far as therapy is concerned in the prevention of vascular colaps and the improvement of the oxemia, oxygen is very useful when there is a venous congestion (clinically, X rays, and oxemia). When the concentration of O2 is lower than 50% in the cases with slight cardiac failure; do not use oxygen in higher concentrations unless the hypoxia is associated to acute pulmonary edema and shock. Mechanic ventilators, and intermitent possitive pressure are recommended even though they have a posenous effect on the cardiac output. Always keep the air ways permeable: changing position, breathing exercises, humidifications, aspiration of secretions, intubation, or traqueostomy depending upon the various cases.     

Accelerated idioventricular rhythm in acute myocardial infarct]

A continuous (for 24 hours) ECG recording on a magnetic tape with its subsequent decodification on a special analyser was performed in 31 patients with acute myocardial infarction during the 1st day of the onset of the disease in order to reveal an accelerated idioventricular rhythm and ventricular tachycardia. An accelerated idioventricular rhythm was found to occur within the 1st and early during the 2nd day of the disease in 29% of the patients. The importance of some factors, that of the sinus rhythm rate in particular, was studied with reference to the development of an accelerated idioventricular rhythm. The causes of its development are discussed, as well as those of its disappearance, interrelationship with ventricular tachycardia, and the prognostic importance of the accelerated idioventricular rhythm recorded throughout a 3-month observation and its place in the differential diagnosis in acute myocardial infarction.     

Rupture of the interventricular septum in acute myocardial infarct]

Ventricular septal rupture in patients with acute myocardial infarction is not a common complication. It was found in 20 patients of 4298 admitted to the coronary care unit of the Instituto Nacional de Cardiología Ignacio Chávez from January 1980 to March 1991. The diagnosis was made by right heart catheterization if 85%, by echocardiography in 35% and by postmortem study in 15% of the patients. Mortality was 70%. In all patients the functional class worsened after the rupture, from class I to III or IV. There were not significant differences in mortality in relation to risk factors, or hemodynamic findings. Mortality was higher in older patients, females and patients with anterior myocardial infarction. Angiographic studies did not increase mortality and are necessary to establish an early surgical treatment.     

Spasm of the coronary arteries in acute myocardial infarct]

Emergency coronarography was performed in 36 patients with myocardial infarction. Spasms of the coronary artery supplying the area of the infarction were observed in some cases. The fact that the vessel was demonstrated along its entire length after 0.5 mg of nitroglycerine was placed under the tongue confirmed the existence of the spasm. In most patients with acute myocardial infarction the vessel supplying the area of the affected muscle has the appearance of a stump, i.e. its peripheral segments are not demonstrated. At the same time, in some patients, who died some time after the examination, anatomical study of the heart showed that these segments of the vessel were not occluded. Such an angiographic picture may also be explained by the spasm of the coronary arteries. The angiographic pattern of the coronary channel in patients with acute myocardial infarction suggests that coronarolytics and spasmolytics injected both intravenously and into the coronary vessel in coronarography may be used still more extensively.