With the longer life expectancy of the population.

With the longer life expectancy of the population, calcific aortic stenosis has become a customary cardiac problem in the somewhat advanced in life When patients with moderate to censorious aortic stenosis become symptomatic, the prognosis is usually poor in absence of valve replacement and abrupt death is a feared complication. It has been hypothesized that malignant ventricular arrhythmias could be responsible for the high incidence of abrupt death in symptomatic patients with aortic stenosis. The aim of this review is to analyze the prevalence, the electrophysiologic mechanisms, and the possible part of ventricular arrhythmias in the exhibition of symptoms and in the issue of adult subjects with aortic stenosis.

(CHEST 1998; 113:482-91)

Key words: aortic stenosis; electrophysiologic mechanisms; left ventricular hypertrophy; unexpected death; syncope; ventricular arrhythmias

Abbreviations: ACE = angiotensin-converting enzyme; AS = aortic stenosis; EAD = early afterdepolarization; LVH = left ventricular hypertrophy

With the longer life expectancy of the population, calcific aortic stenosis (AS) has become an increasingly prevalent condition. It is well known that AS in the adult has a progressive course with a extended asymptomatic period. However, when inexorable AS becomes symptomatic, the prognosis is usually poor in the absence of valve replacement, with an average survival ranging between 1 and 3 years,[1] because the pair the medical treatment and the balloon valvuloplasty have no other than a short-term efficacy. Furthermore, death observ among symptomatic unoperated-on patients is often sudden, with an incidence ranging from 8 to 34%;[23] reciprocally sudden death appears only occasionally in asymptomatic enthralls (0 to 5% of adult and 75% of children).[1,4,5] It has been hypothesized that malignant ventricular arrhythmias may be responsible for the high incidence of abrupt death in AS patients, as well as in those with coronary artery disease or cardiomyopathy. However, although a higher prevalence of ventricular arrhythmias has been documented in AS patients compared with superintendence subjects, the mechanisms underlying these arrhythmias and their impact forward the natural history of disease are still debated. The sense of this review, is to analyze the prevalence of ventricular arrhythmias and their possible part in the development of symptoms and issue of adult subjects with AS.

Prevalence of Ventricular Arrhythmias in Adult AS

Several studies showed that premature ventricular contractions, documented according to Holter monitoring, are frequent in patients with aortic valvular disease (Table 1) In the early 1980 Santiga et al[6] and von Olshausen et al[7] documented a high prevalence of ventricular arrhythmias in patients with sharp AS and/or aortic regurgitation without significant coronary artery disease. The commonness and complexity of ventricular arrhythmias were closely related to myocardial function and thus were more used by all in patients with higher left ventricular systolic stres and reduc systolic function. forward the contrary the severity of arrhythmias was not related to the etiology valve stenosis, the transvalvular gradient, or the severity of aortic regurgitation.

[TABULAR DATA 1 NOT REPRODUCIBLE IN ASCII]

These observations were later confirmed by the agency of Klein,[8] Kostis et al,[9] and more not long ago by Martinez-Useros et al,[10] Michel et al,[11] and our assemblage (unpublished data). Of interest, in all these studies, no relation was observ between severity of arrhythmias and elision or sudden death during follow-up However, Schwartz et al,[12] in 1969 reported that the ECG of AS patients recorded during elision often documented ventricular tachycardia or on a level ventricular fibrillation reverting to sinus periodical emphasis spontaneously. If the malignant ventricular arrhythmias persisted longer unexpected death eventually occurred. Also, von Olshausen et al[13] have lately described seven AS patients who abruptly died during Holter monitoring; in six of them, the cause of death was a malignant tachyarrhythmia (monomorphic or polymorphic ventricular tachycardia) and alone in one patient was death associated with bradyarrhythmia. Increased ectopic ventricular activity math compages forms (couplets and nonsustained ventricular tachycardia) and a significant acceleration in heart rate were observ within the last hours before tachyarrhythmic unanticipated death, thus reinforcing the hypothesis that a athletic link exists between frequency and complexity of ventricular arrhythmias and risk of unanticipated death in these patients. However, it must be mentioned that all the patients in this contemplation had moderate to severe heart failure and impaired left ventricular systolic function, thus the arrhythmias leading to the unexpected death could be related to the left ventricular dysfunction itself more than to the effusion obstruction.[13]

Mechanism of Ventricular Arrhythmias in AS

Risk of Ventricular Arrhythmias in Left Ventricular Hypertrophy

The Framingham Heart consideration showed that hypertensive patients with left ventricular hypertrophy (LVH) are at increased risk of premature cardiovascular death and this is commonly sudden.[14-16] Accordingly, the hypothesis that ventricular arrhythmias may be responsible for unlooked for death was formulated.[17-20] Nevertheless, the part of ventricular arrhythmias in the pathogenesis of unexpected death in patients with LVH is still unclear. newly Bikkina et al[21] demonstrated that the port of asymptomatic frequent and/or tangled skein ventricular arrhythmias, in subjects with LVH and at liberty of clinically apparent coronary heart disease, is associated with a doubling of all-cause mortality. Coste et al[22] performed programmed ventricular stimulation in patients with essential hypertension with and without LVH in succession echocardiogram. Ventricular stimulation induced intraventricular reentry beats in 92% of hypertensive bring under rules with and only in 17% of those without LVH indicating that the increase in myocardial mass may show an anatomic substrate for ventricular arrhythmias. In 40 hypertensive patients with documented LVH and history of swoon and aborted sudden death, Vester and coauthors[23] performed programmed ventricular stimulation inducing ventricular tachycardia or ventricular fibrillation in 30% of them. Furthermore, it is well known that in patients with hypertrophic cardiomyopathy, the rate of inducibility of ventricular tachycardia is high, ranging between 40% and 82% in different studies.[24,25] These data support the hypothesis that LVH may provide a substrate for malignant ventricular arrhythmias and unlooked for death, independently of the etiology.

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