Repolarization Disturbances Research Articles

ECG Abnormalities in Patients with Sarcoidosis

The frequency and type of some abnormal ECG findings in 86 consecutive patients with intrathoracic sarcoidosis were studied and compared with 86 age- and sex-matched healthy controls. All ECGs from the patients and controls were mixed and evaluated blindly by one of the investigators. Ectopic beats were seen in 6 patients in the sarcoidosis group and in 3 individuals in the control group. Patients with stage III sarcoidosis had more conduction defects compared with stage I and II patients and with the controls. Repolarization disturbances were found in 17 patients and 6 controls. These disturbances were more common in patients with stage I and II than in those with stage III sarcoidosis. The total number of patients with some ECG abnormality was 27 compared to 12 controls.

Electrophysiology and indications for pacing in the '80's.

Newer electrophysiological studies have improved our understanding of the pathogenesis of cardiac arrhythmias. Bradycardias originate either from a dysfunction of impulse formation in the sinoatrial node or from a disturbed conduction of the impulse. Different pathogenetic mechanisms are discussed as causes of tachyarrhythmias: circus movement (re-entry) is primarily due to pathological changes in conduction and refractoriness. Focal impulse formation results from local disturbances of depolarization and repolarization of the cell membrane: increased automaticity, abnormal automaticity, triggered activity. Symptomatic bradycardias still represent the standard indication for cardiac pacing particularly with implantable pacemakers. Based on clinical electrophysiology, various types of pacemakers are available at present: atrial triggered and atrial pacing pacemakers, AV-sequential pacemakers, ventricular demand-pacemakers, stand-by pacemakers, and fixed rate pacemakers. The multiprogrammability of newer pacemaker devices is a very useful tool in avoiding secondary interventions. For antitachycardia pacemaker therapy there are essentially three methods in use: 1. overdrive pacing to prevent re-entry phenomena and automaticity and also to suppress tachyarrhythmias based on increased or abnormal automaticity; 2. competitive stimulation for termination of tachycardias by means of single impulses; and 3. rapid atrial stimulation to convert atrial flutter into atrial fibrillation and consequently to normal sinus rhythm. In very rare cases rapid ventricular stimulation is mandatory. The positive results achieved with temporary stimulation methods have led to the development of permanent (implantable) antitachycardia pacemakers for long-term therapy, which have proven to be a low-risk alternative in drug-resistant tachyarrhythmias.

Ventricular Aneurysms in Acute Experimental Chagas' Myocardiopathy

Of 27 puppies infected with Schizotrypanum cruzi two showed electrocardiographic changes in the ST-T segment and in the T wave compatible with parietal myocardial aneurysms. When the thorax was opened, examination confirmed the presence of aneurysms in the free walls of the heart. In one of the cases, histologic examination of the aneurysm showed myocardial fiber changes. Myocytoiysis was the principal change. In it the main electrocardiographic changes were interpreted as subepicardial injury and ischemia. In the second case, the dominant histologic change consisted of dense and extensive myocardial inflammatory infiltrations, which enlarged the interstitial spaces. There were low voltage of QRS, focal block and disturbances in the ventricular repolarization electrocardiographically. Aneurysmal dilatation in acute experimental Chagas' myocarditis appears to be caused by fiber lesions, edema and interstitial inflammatory infiltrations. Intracavitary ventricular pressure will produce a convexity of the myocardial wall during systole, which is reduced during diastole.

Pulmonary Edema by Ascending to High Altitudes

Acute pulmonary edema was observed in 36 young healthy persons after ascending to altitudes 13,700 feet or more above sea level. Most of them were born and living permanently at high altitudes and developed pulmonary edema on returning to the mountains after a relatively short stay at lower or sea levels. The clinical manifestations were usually severe and rapidly progressive disappearing in 24 to 48 hours with oxygen administration. The predominant roentgenologic appearance was a coarse mottling exudate, more confluent in both parahilar regions. The heart size remained normal. The electrocardiogram showed acute right ventricular overloading and primary disturbances of repolarization probably related to right ventricular myocardial ischemia. Cardiac catheterization performed in one patient during the recovery period at sea level, revealed normal pressures in the pulmonary artery and capillary bed. Necropsies performed in two patients showed severe pulmonary edema, extensive areas with hyaline membrane, thrombosis of distal arteries and septal capillaries and multiple preterminal arterioles. The left atrium and ventricle were normal and there was a moderate right ventricular hypertrophy usually found in the high altitude resident. Pulmonary edema of high altitude appears to be the result of a magnification of the hemodynamic changes occurring during a rapid exposure to an environment of hypoxia and low temperature. These changes would be an increase in cardiac output and pulmonary blood volume, pulmonary vasoconstriction at pre-capillary level with secondary pulmonary hypertension, and increased pulmonary capillary permeability.