Markers of electrical instability in hypertensive patients with and without ventricular arrhythmias. Are they useful in identifying patients with different risk profiles?

BACKGROUND: Markers of electrical instability of the ventricular myocardium, namely abnormal repolarization and late potentials, are frequently observed in patients with hypertension when both ventricular arrhythmias and left ventricular hypertrophy are present. This information cannot be extrapolated to the population of hypertensive patients with ventricular arrhythmias but without left ventricular hypertrophy. OBJECTIVE: To evaluate QT duration, QT dispersion and the incidence of ventricular late potentials in patients with essential hypertension, already on anti-hypertensive therapy, both with and without non-sustained ventricular arrhythmia. DESIGN: The study population consisted of 49 patients with essential hypertension who were compared to 89 control normotensive subjects both with and without frequent (> 30 per h) ventricular ectopic beats (VPBs). Patients were divided into four groups: (1) hypertensive patients without VPBs (H, n = 19), (2) hypertensive patients with VPBs (HA, n = 30), (3) normotensive subjects without VPBs (C, n = 28), and (4) normotensive subjects with VPBs (CA, n=61). METHODS: Echocardiographic parameters, QT interval, QT dispersion and signal-averaged ECG were evaluated without withdrawing anti-hypertensive drugs. RESULTS: In no case was left ventricular hypertrophy documented. The number of VPBs during 24 h Holter recording (median 11 343 versus 7617) and the incidence of repetitive VPBs (37 versus 46% of patients) were similar in the two groups of patients (HA versus CA). Signal-averaged ECG parameters were normal and not different between the four groups. QT interval was longer in hypertensive patients compared to controls irrespective of the presence of VPBs. QT dispersion was slightly greater in subjects with VPBs, both hypertensive and normotensive, compared to subjects without arrhythmias. CONCLUSIONS: In patients with hypertension well-controlled by drug therapy and without left ventricular hypertrophy, frequent VPBs are not associated with markers indicating an electrophysiological substrate for re-entrant arrhythmias. However, QT prolongation suggests the persistence of a higher risk of cardiovascular mortality that is independent of the presence of VPBs.

Increased left ventricular dimensions in patients with frequent nonsustained ventricular arrhythmia and no evidence of underlying heart disease.

INTRODUCTION: To test the hypothesis that frequent nonsustained ventricular premature beats (VPBs) in patients without underlying heart disease are the first marker of mild systolic dysfunction of the left ventricle, we evaluated whether a subclinical abnormality of left ventricular function and/or an intraventricular conduction defect was present at the first clinical documentation of the arrhythmia. METHODS AND RESULTS: We compared 57 patients (mean age 46 +/- 14 years) with > 30 VPBs/hour and no heart disease (A) to 32 healthy volunteers (mean age 42 +/- 12 years) without arrhythmia (B). Left ventricular echocardiographic parameters and signal-averaged ECG were evaluated. Filtered QRS duration (98 +/- 10 msec in A vs 98 +/- 7 msec in B) was similar in the two groups. End-diastolic left ventricular diameter (EDLVD) was 50 +/- 6 mm in A versus 47 +/- 3 mm in B (P < 0.005); 15 patients (26%) and none of the controls had EDLVD > or = 55 mm (P < 0.005). Filtered QRS interval was longer in the subgroup of patients (n = 15) with increased EDLVD (> or = 55 mm) compared with the subgroup (n = 42) with EDLVD < 55 mm (106 +/- 9 msec vs 95 +/- 9 msec; P < 0.001) and was related to greater left ventricular mass. CONCLUSION: We documented a subclinical but significant increase of left ventricular dimensions that suggests that frequent VPBs may be an initial marker of mild systolic dysfunction of the left ventricle. However, an effect of VPBs per se in modifying left ventricular dimensions cannot be excluded.