Hypertension is a major public health problem due to its high prevalence and significant complications. It is an important risk factor for sudden cardiac death, of which the incidence increases with increases in blood pressure1).

Great attention has been given to arrhythmias in hypertensive patients. The presence and the complexity of both supraventricular and ventricular arrhythmias have been shown to influence the morbidity, mortality, and quality of life of hypertensive patients2,3). These arrhythmias have a wide spectrum which ranges from supraventricular premature complexes to ventricular tachyarrhythmia or sudden cardiac death. Multiple risk markers for an arrhythmic substrate, which can be applied to hypertensive heart disease, have been identified in different pathological cardiovascular conditions. These include diminished heart rate variability4), QT interval dispersion5), and ventricular late potentials4,6,7). A large QT dispersion indicates the presence of a substrate for ventricular tachyarrhythmias, most obviously by a mechanism of re-entry8).

The electrocardiographic QT interval is a measurement of the duration of ventricular repolarization and is sensitive to myocardial ischemia. The interlead variation in the 12-lead ECG is referred to as QT dispersion. QT dispersion is a noninvasive measurement of regional variation in ventricular recovery time.

The Valsalva maneuver is characterized by a significant increase in intrathoracic pressure which is immediately transmitted to all intrathoracic vascular structures. Ventricular arrhythmias are common in patients with volume or pressure overload, such as aortic valve disease9) or dilated cardiomyopathy 10). The intrathoracic pressure change characteristic of the Valsalva maneuver can act as a factor in the triggering of sudden cardiac death. It may be supposed that the mechanism of this event is a change in the normal sequence of repolarization which alters local electrical gradients and is potentially arrhythmogenic11). Many hypertensive patients are at increased risk for sudden cardiac death because the Valsalva maneuver may be performed 10 to 20 times an hour by patients on bed rest as they move in bed, cough, strain to evacuate stool, and carry or lift heavy materials.

However, QT dispersion during the Valsalva maneuver has not yet been properly investigated in hypertensive patients in clinical settings. Therefore, in this study, the change in QT dispersion during the strain phase of the Valsalva maneuver was investigated in hypertensive patients.

QT dispersion is defined as a QT interval variation in the 12-lead surface electrocardiogram and is accepted as a reflection of regional variation in ventricular repolarization12). It has been shown that increased heterogeneity of ventricular repolarization could favor the development of ventricular arrhythmias13,14). Sudden cardiac death is generally considered to be due to arrhythmia, and in patients with coronary heart disease, a strong correlation exists between abnormal wall motion and ventricular arrhythmia15).

LV hypertrophy is considered an independent risk factor for coronary artery disease and cardiovascular complications16). It has been established that coronary artery disease, stroke, and sudden death are more frequent in patients with LV hypertrophy17).

Ichkhan et al.18) suggested that the greater the LV mass, the greater the QT dispersion in hypertensive patients. When compared with patients with hypertension but without a hypertrophied myocardium, a significantly increased QT dispersion was found in the subset of patients with hypertension and LV hypertrophy. Thus, it is not hypertension per se, but LV hypertrophy that creates an increase in QT dispersion.

Oikarinen et al.19) suggested that, in hypertensive patients with electrocardiographic evidence of LV hypertrophy, increases in LV mass index and LV hypertrophy were associated with a prolonged QT interval and increased QT dispersion. These findings suggested that an increased vulnerability to repolarization-related ventricular arrhythmias might partially explain the increased risk of sudden death in hypertensive patients with increased LV mass. A recent study conducted by Oikarinen et al.20) suggested that, in hypertensive patients with electrocardiographic evidence of LV hypertrophy, regression of echocardiographically determined LV mass and electrocardiographic indexes of LV hypertrophy may partially reduce the QT interval and QT dispersion. The findings presented in this study suggest that QT dispersion, as determined for the standard electrocardiogram, shows an increase of left ventricular mass.

Clearly, the hypertrophic myocardium is a fertile ground for the development and propagation of arrhythmias, which increase the risk of sudden arrhythmic death. A major question then arises: If LV hypertrophy is regressed by effective treatment, is arrhythmic risk decreased? Karpanou et al.21) pronounced that LV hypertrophy is associated with increased QT dispersion in hypertensive patients, whereas QT dispersion can be decreased by the regression of LV hypertrophy either with angiotensin-converting enzyme inhibitors or calcium antagonist therapy.

We examined the acute effects of the strain phase of the Valsalva maneuver, and whether there were significant changes in QT dispersion that explained the arrhythmia formation and sudden death during some conditions which stimulate the Valsalva maneuver, such as constipation, severe coughing spells, vomiting, and carrying or lifting heavy objects. During the strain, the increased intrathoracic pressure obstructs systemic venous return, and the strain phase of the Valsalva maneuver is characterized by a fall in systolic blood pressure and pulse pressure, as well as a decrease in coronary ischemia22,23). Local differences in repolarization and excitability induced by a mechanism as shown by Taggart et al.24) would facilitate arrhythmias by a mechanism of re-entry. Although they were able to exclude whether these were real phenomena or artifacts, early after-depolarizations accompanied by ventricular premature contractions suggested another explanation for arrhythmia24). The findings of this study support that the Valsalva maneuver affects the prolongation of QT dispersion in hypertensive patients, especially stage II patients or patients who are severely hypertensive. This may be due to the increased strain in the myocardia of severely hypertensive patients compared to that of mildly hypertensive patients.

There are some conditions, such as constipation, severe coughing spells, vomiting, and carrying or lifting heavy objects that increase intrathoracic pressure and may increase QT dispersion. Therefore, all of these conditions should be treated appropriately and should be avoided by patients with severe hypertension.