Muerte súbita en el adulto joven sin cardiopatía demostrable: características clínicas y electrofisiológicas en 3 casos / Sudden cardiac death in 3 young patients without overt heart disease

We reported 3 young adult males who developed spontaneous ventricular fibrillation in the abscence of demonstrable heart disease. Extensive clincial and elelcrophysiilogic evaluation failed to disclose a cause for the arrhythmia. Antiarrhythmic drugs were empirically used in all patients but 2 of then eventually died. Thus, unexplained ventricular fibrillation without demonstrable heart disease carries a serious short term prognosis. An implantable cardiovertodefibrillator may be the therapy of choice in these cases

Responses of the QT interval of the electrocardiogram during emotional stress.

The relationship of emotional stress to the duration of the QT interval of the electrocardiogram (which contains the period of repolarization of the myocardium) was explored because QT prolongation has been shown under some circumstances to carry a risk of potentially fatal cardiac arrhythmia. A thoroughly studied case of repeated serious and ultimately fatal arrhythmia which occurred in a setting of overwhelming family and personal stress and which was preceded by marked prolongation of the QT interval prompted an experimental study of the behavior of the QT interval during stressful interviews. The subjects were 17 men and women ranging in age from 26 to 74. The experimental sessions included: 1) a period of inactivity with the subject sitting alone, 2) a period of "neutral" discussion, 3) a period of dwelling on a presumed stressful topic, followed by 4) a period of reassurance. Heart rate, respiration, arterial pressure, and the electrocardiogram were recorded throughout the four intervals together with a real time tracing of the QT interval of the electrocardiogram made by a computerized instrument recently devised by one of us (J.E.). Most of the subjects reacted to the stressful discussion with anger and resentment that was associated with shortening of QT. Two of them, however, who reacted with dejection and a feeling of being overwhelmed, displayed lengthening of QT. The QT changes were generally not linked to changes in heart rate.

Sudden cardiac death: etiologies, pathogenesis, and management.

Sudden death claims an estimated 350,000 lives per year in the United States. When death occurs within 1 hour of the onset of symptoms, 90% are the result of ventricular tachyarrhythmias. The majority of victims are middle-aged men with coronary artery disease, but in approximately 25%, sudden death is the presenting manifestation of their problem. In some populations, the detection of premature ventricular complexes (PVCs) by ambulatory monitoring is predictive of an increased risk of sudden death. However, the arrhythmia that best predicts this risk is unclear, and ambient arrhythmias are only a modest marker of this risk. Therapy to suppress asymptomatic PVCs has not been shown to be effective in preventing sudden death, and in some cases, lethal arrhythmias can be prevented without significant effects on ambient arrhythmias. Other risk markers such as depressed left ventricular function and the presence of low-amplitude, long-duration, late potentials recorded on a signal averaged electrocardiogram are more powerful predictors of risk than are PVCs. These latter findings in particular support the presence of areas of slow electrical conduction (a requirement for reentrant mechanism arrhythmias) and suggest that an abnormal electrical environment or "substrate" is the most important factor in this problem. The management of patients at risk for sudden death is controversial. While postinfarct survivors with arrhythmias constitute a population at increased risk, the absolute risk is only about 5% in the first year and has not been shown to be improved by conventional antiarrhythmic drugs. Small study size, arrhythmia variability, ill-defined end points, and proarrhythmia may partially explain this apparent lack of efficacy. The prophylactic use of antiarrhythmic drugs other than beta-blockers to prevent sudden death in asymptomatic populations at risk is therefore of unproven benefit. By contrast, patients who have survived a life-threatening arrhythmia unrelated to an acute myocardial infarction have an approximately 30% risk of recurrence in the following year. In these patients, the use of ambulatory monitoring to guide therapy is limited by the high incidence of false-negative responses (lethal arrhythmia recurrence despite ambient arrhythmia suppression) and the lack of frequent spontaneous arrhythmias in many patients. In this patient population, electrophysiological testing can be used to prognosticate recurrence and gain insight into arrhythmia mechanism, stability, and hemodynamic tolerance. The technique is also useful in guiding both pharmacological and nonpharmacological therapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Left ventricular hypertrophy as a factor in arrhythmias and sudden death.

Hypertensive patients with left ventricular hypertrophy (LVH) are predisposed to sudden cardiac death. Several studies have demonstrated that complex ventricular arrhythmias, including episodes of nonsustained ventricular tachycardia, occur commonly during ambulatory electrocardiographic monitoring of hypertensive patients with LVH. The prognostic significance of such arrhythmias is not known. In other forms of cardiac hypertrophy, however, such as hypertrophic cardiomyopathy, complex ventricular arrhythmias detected during ambulatory monitoring are predictive of subsequent sudden death and there is some evidence that appropriate antiarrhythmic drug therapy may reduce mortality.

[Cardiovascular diseases in nocturnal disorders of respiratory regulation]. / Herz-Kreislauf-Erkrankungen bei nächtlichen Atemregulationsstörungen.

Sleep related disorders of respiratory regulation can result, through various mechanisms, in impairment of the hemodynamics of the heart and the systemic and pulmonary circulations. The group of patients with sleep apnea has been most thoroughly investigated thus far. The patients frequently develop essential and/or pulmonary hypertension. In sleep all forms of cardiac arrhythmia may occur, and thus the patients are at high risk for nocturnal sudden cardiac death. Responsibility for most hemodynamic alterations is attributed to apnea-induced hypoxia and hypercapnia and the intrathoracic pressure fluctuations observed in obstructive apnea. However, we are still short of detailed knowledge regarding the individual pathologic mechanisms. The hemodynamic changes observed in patients with sleep related disorders of respiratory regulation lead in the long run to cardiac failure. Early diagnosis and care of these patients is therefore urgently necessary to render timely therapeutic action possible.

Psychiatric aspects of patients with malignant ventricular arrhythmias.

The major cause of cardiac mortality in the United States is sudden cardiac death, most often the result of ventricular tachycardia-ventricular fibrillation. Transient risk factors for sudden cardiac death include psychiatric conditions mediated through the CNS. Major advances in the evaluation and treatment of patients who have survived malignant ventricular arrhythmias have been accompanied by challenging management and therapy issues for the psychiatrist involved in the care of such patients. The authors suggest ways to meet these challenges, especially in the care of patients with concomitant anxiety, depression, delirium, or psychosis.

Atherosclerosis of coronary arteries, coronary heart disease and sudden coronary death.

Correlation between the severity of coronary atherosclerosis, thrombosis and sudden cardiac death was examined in 721 autopsied cases. Severe coronary atherosclerosis with stenosis was found in most of them; however a similar grade of atherosclerosis was discovered in patients with ischaemic heart disease not dying suddenly. Acute coronary thrombosis in the studied subjects was diagnosed post mortem in about 20 percent of those who died suddenly. Other studies indicate frequencies between 4-93%. There was no consistent time dependence.

Cardiac response to submaximal exercise in dogs susceptible to sudden cardiac death.

The hemodynamic response to submaximal exercise was investigated in 38 mongrel dogs with healed anterior wall myocardial infarctions. The dogs were chronically instrumented to measure heart rate (HR), left ventricular pressure (LVP), LVP rate of change, and coronary blood flow. A 2 min coronary occlusion was initiated during the last minute of an exercise stress test and continued for 1 min after cessation of exercise. Nineteen dogs had ventricular fibrillation (susceptible) while 19 animals did not (resistant) during this test. The cardiac response to submaximal exercise was markedly different between the two groups. The susceptible dogs exhibited a significantly higher HR and left ventricular end-diastolic pressure (LVEDP) but a significantly lower left ventricular systolic pressure (LVSP) in response to exercise than did the resistant animals. (For example, response to 6.4 kph at 8% grade; HR, susceptible 201.4 +/- 5.1 beats/min vs. resistant 176.2 +/- 5.6 beats/min; LVEDP, susceptible 19.4 +/- 1.1 mmHg vs. resistant 12.3 +/- 1.7 mmHg; LVSP, susceptible 136.9 +/- 7.9 mmHg vs. resistant 154.6 +/- 9.8 mmHg.) beta-Adrenergic receptor blockade with propranolol reduced the difference noted in the HR response but exacerbated the LVP differences (response to 6.4 kph at 8% grade; HR, susceptible 163.4 +/- 4.7 mmHg vs. resistant 150.3 +/- 6.4 mmHg; LVEDP susceptible 28.4 +/- 2.1 mmHg vs. resistant 19.6 +/- 3.0 mmHg; LVSP, susceptible 122.2 +/- 8.1 mmHg vs. resistant 142.8 +/- 10.7 mmHg). These data indicate that the animals particularly vulnerable to ventricular fibrillation also exhibit a greater degree of left ventricular dysfunction and an increased sympathetic efferent activity.

The electrophysiologic features of sudden death.

Sudden or instantaneous death is nearly always of cardiac origin. The most common mechanism is a severe electrical dysfunction, which is apparent on Holter monitoring tapes. Identifying patients at risk of sudden cardiac death is difficult, and Holter monitoring has proved to be limited in its diagnostic usefulness. However, in patients who have experienced cardiac arrest Holter monitoring has shown that the electrical abnormalities leading to death vary. These abnormalities usually take time to develop, and during this time the cerebral circulation is partially maintained. In this brief period, lasting less than 2 minutes, the individual may become aware that something is wrong and have time to react.

Timing, mechanism and clinical setting of witnessed deaths in postmyocardial infarction patients.

The temporal distribution and mechanism of death were studied in a large multicenter secondary prevention trial (Aspirin Myocardial Infarction Study) in which acute witnessed death represented 72% (270 of 376) of the deaths due to arteriosclerotic heart disease. Instantaneous deaths represented 28.9% (78 of 270) of the acute witnessed deaths; 45.2% (122 of 270) occurred in the first hour after the onset of symptoms and were defined as sudden deaths. In the subsequent 23 hours, an additional 113 deaths (41.8%) occurred and were defined as intermediate deaths; 29 late deaths (10.7%) occurred after 24 hours. Cardiac arrhythmia was the mechanism of death in 83% (194 of 235) of deaths within 24 hours. Univariate analysis of baseline clinical and electrocardiographic characteristics indicates that a history of congestive heart failure, cardiomegaly, angina pectoris, multiple myocardial infarctions and therapy with digitalis and nitroglycerin were more common in those who died than in survivors, regardless of the timing of death.

Documented sudden cardiac death in prolonged QT syndrome.

Documentation of the mechanism of sudden death is described in a patient with a prolonged QT interval. Ventricular tachycardia was initiated by a ventricular premature beat (VPB) with a prematurity index similar to previous isolated VPBs. This event occurred despite the fact that the patient was receiving phenytoin sodium, a drug known to shorten the QT interval.