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Transient myocardial ischaemia in hypertensives: missing link with left ventricular hypertrophy

S Scheler1, W Motz, B E Strauer

  • 1Medical Clinic B, Heinrich-Heine-University of Düsseldorf, Germany.

European Heart Journal
|September 1, 1992
PubMed

Insights

Transient myocardial ischemia in hypertensive patients with normal coronary angiograms is not linked to increased left ventricular mass. Microcirculation alterations, not myocardial factors, likely cause these ischemic episodes detected by ST Holter monitoring.

Area of Science:

  • Cardiology
  • Hypertension Research
  • Diagnostic Electrocardiology

Background:

  • Hypertensive patients frequently report angina pectoris despite normal coronary angiograms.
  • The underlying cause of this angina, particularly transient myocardial ischemia, requires further investigation.

Purpose of the Study:

  • To determine if electrocardiographical signs of transient myocardial ischemia during 24-hour ST Holter monitoring correlate with increased left ventricular muscle mass in hypertensive patients.

Main Methods:

  • Studied 35 hypertensive patients and 9 normotensive controls using 24-hour ST Holter monitoring.
  • Utilized M-mode and two-dimensional echocardiography to assess left ventricular muscle mass.
  • Compared hypertensive patients with and without ST-segment depression.

Main Results:

  • No significant difference in blood pressure or left ventricular muscle mass was observed between hypertensive patients with and without ST-segment depression.
  • Both groups exhibited borderline left ventricular hypertrophy, suggesting myocardial factors are not primary drivers of ST depression.

Conclusions:

  • Increased left ventricular muscle mass is not associated with transient myocardial ischemia indicated by ST-segment depression in hypertensive patients.
  • Functional and structural changes at the microcirculation level are likely responsible for transient ST-segment depression episodes.

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