The American journal of cardiology
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A direct, continuous, and independent relation between blood pressure and the incidence of various cardiovascular events, such as stroke and myocardial infarction, is now well accepted. The increase in risk can be attributed to structural and functional changes in target organs. Central to many of these pathophysiologic processes is the renin-angiotensin system (RAS), specifically, angiotensin II. ⋯ Angiotensin-converting enzyme (ACE) inhibitors interrupt the RAS by preventing the conversion of angiotensin I to angiotensin II. They also increase plasma levels of bradykinin, which possesses vasodilatory and tissue-protective properties. The combination of an AT(1) receptor antagonist with an ACE inhibitor represents an appealing therapeutic strategy, because it should produce more complete blockade of the RAS, while preserving the beneficial effects mediated by AT(2) receptor stimulation and increased bradykinin levels.
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Meta Analysis
From the HOPE to the ONTARGET and the TRANSCEND studies: challenges in improving prognosis.
The Heart Outcomes Prevention Evaluation (HOPE) study conclusively demonstrated that ramipril, an angiotensin-converting enzyme (ACE) inhibitor, reduces the risk of cardiovascular death, myocardial infarction (MI), and death in patients at risk for cardiovascular events but without heart failure. The Study to Evaluate Carotid Ultrasound Changes in Patients Treated with Ramipril and Vitamin E (SECURE) substudy demonstrated that ramipril also reduced atherosclerosis. These results suggest that the renin-angiotensin system (RAS) has a more important role in the development and progression of atherosclerosis than previously believed, and they indicate the need for further clinical studies to define the range of benefits available from modifying the RAS. ⋯ The primary endpoint for both trials is a composite of cardiovascular death, MI, stroke, and hospitalization for heart failure. Secondary endpoints will investigate reductions in the development of diabetes mellitus, nephropathy, dementia, and atrial fibrillation. These 2 trials are expected to provide new insights into the optimal treatment of patients at high risk of complications from atherosclerosis.
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Why adults with the Eisenmenger syndrome fare so much better than other patients with severe pulmonary hypertension is not known, but may be related to unique hemodynamics found only in these patients and in normal fetuses. We used echocardiography to evaluate ventricular morphology and function in 80 subjects: 45 cyanotic adults and 5 cyanotic adolescents with Eisenmenger syndrome, 10 infants with nonrestrictive ventricular septal defect and left-to-right shunt flow (pre-Eisenmenger phase), and 20 fetuses with structurally normal hearts. Cross-sectional morphology of the hearts was the same in all 4 groups with a flat ventricular septum throughout the cardiac cycle and equal thickness of the right and left ventricular free walls (regression slope 0.98, r = 0.97, p <0.0001). ⋯ Overall, there was a highly significant linear relation between right and left ventricular function (r = 0.81, p <0.0001). The hearts of patients with Eisenmenger syndrome are more like normal fetal hearts than normal adult hearts. Because of the unique cardiovascular hemodynamics, regression of right ventricular wall thickness does not occur and is likely the reason that patients with Eisenmenger syndrome fare so much better than other adults with severe pulmonary hypertension.