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[The dipyridamole-echo-ECG test in hypertensives with microvascular angina]
Insights
Essential hypertension patients with chest pain and normal coronary arteries often experience "silent" angina during dipyridamole-echocardiography tests (DET). Left ventricular hypertrophy is not required for this induced angina.
Area of Science:
- Cardiology
- Hypertension Research
- Diagnostic Imaging
Context:
- Microvascular angina, characterized by chest pain despite normal coronary arteries, is observed in essential hypertension.
- This condition is associated with the development of left ventricular hypertrophy.
- The Dipyridamole-Echocardiography Test (DET) is used to assess cardiac function under pharmacological stress.
Purpose:
- To evaluate the occurrence of "echocardiographically silent" angina and ST segment depression during DET in essential hypertensive patients with chest pain and normal coronary arteries.
- To determine if left ventricular hypertrophy is a prerequisite for inducible angina in this patient group.
Summary:
- Dipyridamole-Echocardiography Test (DET) was performed on 28 essential hypertensives with chest pain and normal coronary arteries, and 12 healthy controls.
- Essential hypertensives showed significantly higher rates of ST depression (54% vs 17%) and chest pain (57% vs 17%) during DET compared to controls.
- Left ventricular hypertrophy was present in 9 essential hypertensives but did not correlate with the induction of chest pain or ST depression.
Impact:
- Essential hypertensive patients with chest pain and normal coronary arteries frequently exhibit inducible angina or ST depression during DET, even without echocardiographic evidence of left ventricular hypertrophy.
- These findings highlight the utility of DET in diagnosing microvascular dysfunction in hypertensive patients.
- The study suggests that left ventricular hypertrophy is not essential for the manifestation of dipyridamole-induced angina in this population.
Abstract:
Microvascular angina - chest pain syndrome in the presence of angiographically normal epicardial coronary arteries and reduced flow reserve - has been also described in patients with essential hypertension and it has been linked to the development of left ventricular hypertrophy. Dipyridamole-Echocardiography Test (DET: 2D-echo and 12 lead ECG monitoring with dipyridamole infusion, up to 0.84 mg/kg over 10') was performed in 28 essential hypertensives meeting the following inclusion criteria; 1) history of chest pain; 2) angiographically normal coronary arteries; 3) normal resting regional and global left ventricular function. A group of 12 (age and sex matched) normotensives with the same inclusion criteria, as well as with negative exercise stress test, was also evaluated. During DET, none, either in essential hypertensives or in control group, developed a regional dyssynergy of contraction; 15 in essential hypertensives, and 2 in control group had a diagnostic (greater than 0.1 mVolt from baseline) ST segment depression on ECG tracing (54 vs 17% p less than 0.01); 16 in essential hypertensives and 2 in control group had chest pain (57 vs 17%, p less than 0.01). None of the control group and 9 of the essential hypertensives had echocardiographically assessed left ventricular hypertrophy. In the essential hypertensives group, ventricular hypertrophy was present in 7/20 patients with and in 2/8 patients without dipyridamole induced chest pain and/or ST segment depression (35 vs 25%, p = ns). In conclusion, essential hypertensives patients with chest pain and angiographically normal coronary arteries frequently show "echocardiographically silent" angina and/or ST segment depression during DET. The presence of ventricular hypertrophy does not appear to be a prerequisite for the induction of angina in these patients.