Left ventricular dysfunction secondary to ischemia in women with angina and normal coronary angiograms.

BACKGROUND: Microvascular disease is proposed as a cause of segmental myocardial blood flow abnormalities and heterogeneous myocardial perfusion in cardiac syndrome X. OBJECTIVE: To assess if myocardial ischemia can be evidenced through both perfusion abnormalities and poststress left ventricular ejection fraction (LVEF) reduction by gated single photon emission tomography (SPECT) myocardial scintigraphy in women with syndrome X in a similar way to those with epicardial coronary lesions. METHODS: Three groups of postmenopausal women were studied: group I, 20 women with angina, perfusion defects, and normal coronary angiography; group II, 20 women with epicardial coronary lesions (> or =50% of coronary lumen reduction); group III, 15 volunteers without signs or symptoms of ischemia (control group). Each underwent technetium-99m ((99m)TC) methoxyisobutylisonitrile gated SPECT myocardial scintigraphy (protocol: exercise-stress-rest), brachial artery endothelial function measured by ultrasonography, and lipidogram. RESULTS: Groups I and III patients had a higher body mass index (BMI). There were more smokers in groups I and II. Very low density lipoprotein cholesterol (VLDL-C) and triglycerides were higher in group II patients. The brachial artery vasodilator responsiveness after 5 minutes of ischemia was similarly lower in patients of groups I and II compared with those of group III (3% vs. 6.5%, respectively; p = 0.03 group III vs. group I and group II). Mean DeltaLVEF (LVEF poststress minus LVEF at rest) was -3.86%, -2.90%, and 4.18% in groups I, II, and III, respectively (p = NS between I and II, p = 0.005 between II and III, and p = 0.003 between I and III). In 43% of group I patients and in 10 of 18 group III patients with perfusion defects, there was a poststress LVEF reduction >5%. CONCLUSIONS: Stress-induced ischemia is associated with poststress LVEF reduction as a probable manifestation of myocardial stunning in postmenopausal women with typical angina and normal coronary angiography.

Ischemia in women with angina and normal coronary angiograms.

BACKGROUND: Coronary artery disease is frequent in postmenopausal women. Myocardial ischemia has been induced with stress testing, and a relationship between endothelial dysfunction and perfusion defects has been reported. OBJECTIVE: To evaluate whether myocardial ischemia can be evidenced both by perfusion and function abnormalities using gated single-photon emission computed-tomography myocardial scintigraphy with technetium-labeled compounds in women with typical angina, normal coronary angiography, and endothelial dysfunction. METHODS AND RESULTS: Fifty-nine postmenopausal patients were studied. Each underwent technetium-99m methoxy-isobutyl-isonitrile myocardial scintigraphy (protocol: exercise stress-rest), brachial artery endothelial function measured by ultrasonography, lipidogram, and 24-h ambulatory ECG recording (Holter). Twenty-one patients (group I) showed perfusion defects in myocardial scintigraphy, whereas the other 38 patients (group II) did not. Group I patients exhibited endothelial dysfunction more frequently (57 vs. 29%) than those of group II. Among group I patients, 12 showed a reversible perfusion defect that, in 75% of the cases, was associated with poststress left ventricular ejection fraction reduction greater than 5% and a regional hypokinesis. Nine patients had fixed defects, which in 56% of the cases were associated with poststress left ventricular ejection fraction reduction greater than 5%. Left ventricular ejection fraction poststress minus left ventricular ejection fraction at rest was -5.2% in group I patients versus -1.8% in group II (P<0.001). Three patients in group I showed evidence of ischemia by Holter compared with four in group II. CONCLUSION: Stress-induced ischemia is associated with poststress left ventricular ejection fraction reduction in postmenopausal women with typical angina, normal coronary angiography, and a trend toward abnormal endothelial-mediated vasodilation.

ACE I/D polymorphism study in a Cuban hypertensive population.

BACKGROUND: The angiotensin converting enzyme (ACE) is a key protein of the renin angiotensin system, whose main function is the conversion of angiotensin I to II. ACE is involved in the physiological control of blood pressure and it is a candidate gene for essential hypertension in humans. We tested the relevance of the ACE insertion/deletion (I/D) polymorphism in our population. METHODS: We recruited 243 hypertensive and 407 normotensive subjects in the city of Havana, matched according to age, sex and ethnic group. The ACE (I/D) polymorphism was determined by the polymerase chain reaction (PCR) technique. The fit of genotype frequencies to Hardy-Weinberg proportions was evaluated in all groups analyzed. The possible association between the ACE I/D polymorphism and hypertension status was tested by chi2 and odds ratio tests. RESULTS: All groups but black female cases were in Hardy-Weinberg equilibrium. The frequencies of the D allele in hypertensive/normotensive subjects were 0.61/0.59 in white males, 0.58/0.58 in white females, 0.47/0.59 in black males and 0.58/0.54 in black females. The distribution of ACE genotypes differed significantly between cases and controls only in black women according to the additive model (chi2p=0.04) but the adjusted OR did not show significant association (OR 1.14 95% CI 0.62 to 2.10). CONCLUSION: The ACE I/D polymorphism was not associated with hypertension in our multiethnic sample. While the chi2 test for additive model in black women suggested a marginal significance, the adjusted OR did not show any significant association.