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Hypertension and sudden death. Increased ventricular ectopic activity in left ventricular hypertrophy
Insights
Hypertensive patients with left ventricular hypertrophy experience more ventricular arrhythmias. Early detection via electrocardiographic monitoring is crucial for identifying high-risk individuals needing aggressive treatment.
Area of Science:
- Cardiology
- Clinical Electrophysiology
Background:
- Left ventricular hypertrophy (LVH) is an independent risk factor for sudden death and myocardial infarction.
- Hypertension is a primary cause of left ventricular hypertrophy.
Purpose of the Study:
- To detect and quantify cardiac arrhythmias in hypertensive patients with left ventricular hypertrophy.
- To assess the relationship between left ventricular hypertrophy and ventricular arrhythmias.
Main Methods:
- 24-hour ambulatory electrocardiographic (ECG) monitoring and arterial pressure recordings.
- Comparison of arrhythmias in normotensive subjects, hypertensive patients without LVH, and hypertensive patients with LVH.
- Measurement of urinary norepinephrine excretion.
Main Results:
- Patients with left ventricular hypertrophy showed significantly more ventricular premature contractions than other groups.
- Five patients with LVH had >30 premature ventricular contractions/minute.
- No significant difference in urinary catecholamine excretion was observed among groups.
Conclusions:
- Left ventricular hypertrophy is associated with increased ventricular arrhythmias.
- Electrocardiographic monitoring can identify high-risk patients with LVH.
- Aggressive therapeutic intervention is recommended for high-risk individuals.
Abstract:
The present study was designed to detect and quantify cardiac arrhythmias in hypertensive patients with left ventricular hypertrophy. Continuous ambulatory electrocardiographic tracings and arterial pressure were recorded for 24 hours in 14 normotensive subjects, 10 patients with established essential hypertension without left ventricular hypertrophy, and 16 hypertensive patients with left ventricular hypertrophy by electrocardiographic criteria. Urinary excretion of norepinephrine was simultaneously measured over four successive four-hour and one eight-hour period. Patients with left ventricular hypertrophy had significantly more ventricular (but not atrial) premature contractions than those without left ventricular hypertrophy or than normotensive subjects. Five patients with left ventricular hypertrophy had episodes of more than 30 premature ventricular contractions per minute. Higher-grade ventricular ectopic activity such as coupled premature ventricular contractions was seen in two, and multifocal premature ventricular contractions were seen in three in the group with left ventricular hypertrophy. No difference in urinary catecholamine excretion rates among the three groups was seen. Left ventricular hypertrophy has been shown to be an independent risk factor for sudden death and acute myocardial infarction. Electrocardiographic monitoring of patients with left ventricular hypertrophy allows identification of those who have the highest risk and, therefore, require the most aggressive therapeutic intervention.