Natsuko Yui

Vasodilator therapy with a new stable prostacyclin analog, OP-41483, for congestive heart failure due to coronary artery disease and comparison of hemodynamic effects and platelet aggregation with nitroprusside

A new stable prostacyclin analog, OP-41483, was used in patients with severe congestive heart failure (CHF) due to coronary artery disease and compared with nitroprusside. During infusion of both drugs, mean brachial arterial pressure, total pulmonary resistance, pulmonary artery wedge pressure and systemic vascular resistance decreased significantly. Cardiac index and stroke index also increased significantly. Platelet aggregation did not change significantly during nitroprusside but decreased significantly with OP-41483 infusion. Thus, this analog may be useful for treatment of patients with CHF due to coronary artery disease.

Reverse remodeling and improved function by antihypertensive treatment in hypertensive patients with coronary artery disease.

Background Although antihypertensive therapy reduces cardiovascular events, it is unclear whether there are differences in cardiac remodeling and function between treatments with nifedipine retard and angiotensin-converting enzyme inhibitors (ACE-Is). It is also not clear how antihypertensive therapy influences cardiac remodeling and function. Methods Hypertensive patients with coronary artery disease were randomly assigned to the nifedipine retard (n = 108) or ACE inhibitors groups (n = 102) and treated for 3 years. The primary endpoints were changes in end-diastolic volume index (EDVI) and end-systolic volume index (ESVI) as indices of cardiac remodeling, whereas the secondary endpoints were changes in ejection fraction (EF), stroke volume index (SVI), cardiac index (CI) and regional wall motion as indices of cardiac function. Left ventriculography was performed at baseline and after 3 years of treatment. Fifty-eight and 61 patients, respectively, were subjected to the final analysis. Results Comparable changes in remodeling and function were obtained in the nifedipine retard group and the ACE-Is group. Both groups showed a significant reduction of EDVI and ESVI, and a significant increase in EF, SVI, and CI, whereas the decreased regional wall motion significantly improved. In both groups, weak but significant correlations were noted between treatment-induced changes of systolic blood pressure and those of primary and secondary endpoints. Conclusion The above findings show that treatments with nifedipine retard or ACE-Is cause a comparable change in remodeling and cardiac function. Lowering of the blood pressure by either drug leads to reverse remodeling or improvement of cardiac function. In addition to alleviation of coronary artery damage by reducing blood pressure, there is a favorable effect on the left ventricular structure and function. Reducing the blood pressure is critically important for hypertensive patients with coronary artery disease.