The long QT syndromes: a critical review, new clinical observations and a unifying hypothesis.

The long QT syndrome

Psychological stress and fatal heart attack: the athens (1981) earthquake natural experiment

In the industrially developed countries, sudden cardiac death is the leading cause of death. It was recognized at the dawn of recorded history and even depicted in Egyptian relief sculpture from the tomb of a noble of the Sixth dynasty approximately 4,500 years ago. Sudden cardiac death has left no age untouched. Sparing neither saint nor sinner, it has burdened man with a sense of uncertainty and fragility. The enormity of this problem demands attention. In the United States, sudden cardiac death claims about 1,200 lives daily, or approximately one victim every minute. It is the leading cause of death among men aged 20 to 64 years, accounting for 32 percent of the fatalities in this group. Nearly 25 percent of persons dying suddenly have had no prior recognized symptoms of heart disease.The excess of widows observed in retirement communities is accounted for by the three- to fourfold greater incidence of sudden cardiac death among men. Sudden death in old age might be a blessing rather than a scourge, but instead it frequently explodes a man's life at its prime, at a median age of only 59 years. The medical profession has sensed the issue but has largely ignored sudden death as a problem amenable to solution. This indifference has not been the result of a lack of interest or concern but a reflection of the belief that sudden cardiac death was the inevitable culmination of coronary atherosclerosis. Because sudden death was unpredictable and afflicted the apparently healthy subject outside the hospital, the physician considered it an act of fate before which he was largely helpless. The advent of the coronary care unit has promoted a reassessment of this complex problem. It has become clear that sudden death is not the inexorable culmination of advanced coronary atherosclerosis but instead is the result of ventricular fibrillation and therefore is readily reversible. 7,8 If ventricular fibrillation were only the consequence of severe coronary atherosclerosis, once reversed it would promptly recur. However, patients treated for ventricular fibrillation seldom have recurring episodes, and they usually recover and survive for long periods. 9,10 The new concept that ventricular fibrillation is an electrical accident suggests that its cause is not anatomic and thereby contributes to the growing interest in redefining the basis for sudden death and developing methods for its containment. Until recently our inability to deal with sudden cardiac death has not been due to a gap in the application of knowledge but to a gap in knowledge itself. The purpose of this review is to indicate how much we know and to sketch the path of possible further progress.

Sudden cardiac death: the major challenge confronting contemporary cardiology.

Abnormalities of sleep are extremely common in critically ill patients, but the mechanisms are poorly understood. About half of total sleep time occurs during the daytime, and circadian rhythm is markedly diminished or lost. Judgments based on inspection consistently overestimate sleep time and do not detect sleep disruption. Accordingly, reliable polygraphic recordings are needed to measure sleep quantity and quality in critically ill patients. Critically ill patients exhibit more frequent arousals and awakenings than is normal, and decreases in rapid eye movement and slow wave sleep. The degree of sleep fragmentation is at least equivalent to that seen in patients with obstructive sleep apnea. About 20% of arousals and awakenings are related to noise, 10% are related to patient care activities, and the cause for the remainder is not known; severity of underlying disease is likely an important factor. Mechanical ventilation can cause sleep disruption, but the precise mechanism has not been defined. Sleep disruption can induce sympathetic activation and elevation of blood pressure, which may contribute to patient morbidity. In healthy subjects, sleep deprivation can decrease immune function and promote negative nitrogen balance. Measures to improve the quantity and quality of sleep in critically ill patients include careful attention to mode of mechanical ventilation, decreasing noise, and sedative agents (although the latter are double-edged swords).

https://link.springer.com/content/pdf/10.1007%2Fs00134-003-2030-6.pdf

Sleep in the intensive care unit

A patient is described having syncopal attacks on being awakened from sleep by auditory stimuli. The electrocardiogram registered during these episodes showed Q-T-segment changes followed by ectopic ventricular activity and spontaneously ending attacks of ventricular fibrillation. Aside from the attacks, her ECG only showed abnormalities of the S-T segment with marked U waves. Hemodynamic and electrophysiologic studies showed no abnormalities. Coronary angiograms were normal. Following therapy with propranolol and diphenylhydantoin she has been free from syncopal episodes for the past 11 months. The mechanism responsible for the Q-T-segment changes and ventricular tachyarrhythmias is not understood.

Aart Vermeulen

Papers

Ventricular fibrillation occurring on arousal from sleep by auditory stimuli