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Silent myocardial ischemia in patients with essential hypertension
A P Yurenev1, V DeQuattro, P B Dubov
1Institute of Clinical Cardiology, Russian Academy of Medical Sciences of the USSR, Moscow.
Insights
Essential hypertension (EH) patients with silent ischemia show elevated norepinephrine and beta-endorphin levels. Different mechanisms underlie coronary insufficiency in these patients, impacting the hypertensive heart.
Area of Science:
- Cardiology
- Internal Medicine
- Hypertension Research
Background:
- Essential hypertension (EH) is a prevalent condition often associated with cardiac complications.
- Silent myocardial ischemia, characterized by painless ST-segment depression, is a significant concern in EH patients.
- Understanding the underlying pathogenetic mechanisms of coronary insufficiency in EH is crucial for effective management.
Purpose of the Study:
- To investigate the significance of the
Main Methods:
- Electrocardiogram (ECG) Holter monitoring in 61 patients with EH stage II.
- Echocardiography, treadmill tests, and transesophageal pacing in patients with silent ST-segment depression.
- 201Tl stress scintigraphy, coronary angiography, platelet aggregation tests, and catecholamine/beta-endorphin measurements during silent ischemia in a subset of patients.
Main Results:
- Silent ST-segment depression was detected in 34 EH patients.
- 201Tl scintigraphy revealed perfusion defects, categorized into two groups based on clearance abnormalities.
- Group I patients exhibited more severe left ventricular hypertrophy (LVH) and higher platelet aggregation; Group II showed less pronounced LVH but more coronary atherosclerosis. Norepinephrine and beta-endorphin levels increased during silent ischemia in both groups.
Conclusions:
- Coronary insufficiency in EH patients with silent ischemia involves diverse pathogenetic mechanisms.
- Left ventricular hypertrophy and platelet aggregation play roles, alongside coronary atherosclerosis.
- Elevated norepinephrine and beta-endorphin levels during silent ischemic episodes suggest neurohormonal involvement.
Abstract:
The aim of this study was to determine the significance of the "coronary factor" in patients with essential hypertension (EH). Electrocardiogram Holter monitoring was performed in 61 patients with EH stage II (according to the World Health Organization criteria). Silent, ie, painless ST-segment depression, was found in 34 patients on whom echocardiography, a treadmill test, and transesophageal pacing were performed. In 21 patients with EH and silent ischemia, the examination included 201Tl stress scintigraphy, coronary angiography, and a platelet aggregation test. In 15 patients, catecholamines and beta-endorphins were obtained in blood samples during silent ischemia. 201Tl scintigraphy showed transient defects of perfusion without clearance abnormalities (group I) and with clearance abnormalities (group II). The patients in group I had more severe left ventricular hypertrophy (LVH) and a significantly higher platelet aggregation response to 0.5 mumol/L adenosine diphosphate; one patient in this group had coronary atherosclerosis. LVH and the platelet aggregation response was less pronounced in the patients in group II, but atherosclerotic lesions of a coronary artery were observed in four patients. In both groups, norepinephrine and beta-endorphin levels were increased during silent episodes of ischemia. The results suggest that there are different pathogenetic mechanisms of coronary insufficiency in patients with EH, a hypertensive heart, and silent ischemia.