PP.21.28

Abstract

Objective: In cases of hypertrophic non obstructive cardiomyopathia a diastolic relaxation disorder as a sign of left ventricular dysfunction is well known. The analysis of the diastolic relaxation disorder is possible by using doppler ultrasonography without interference of the patient, who can report subjectively about dyspnoea and angina pectoris equivalent. An influence on the diastolic relaxation disorder may be induced by the drug ranolazine. Ranolazine inhibits the ischemic generated late sodium influx (I Na late) and reduces consequently the ischemic induced intracellular sodium and calcium overload. On this mechanism the calcium effected diastolic left ventricular wallaclampsia will be decreased. The agency of ranolazine is similar to the calcium antagonists, however without influencing blood pressure and heart rate. Design and method: In this context we report a 56-year-old hypertensive patient with increasing dyspnoea under exercise, weakness and angina counterparts. A hypertrophic non obstructive cardiomyopatia (type I according to Maron) with pronounced diastolic dysfunction could be secured within the framework of the complete diagnosis. After enlightenment we administered ranolazine (Ranexa 375 mg, twice a day). A tissue doppler echocardiography measurement was performed before and under the additional ranolazine therapy. Results: Ijn the entire observation period, the cardiovascular parameters were stable, normotonic, and normofrequent. The patient reported an increased quality of life. After 7 days an improvement of the E‘A‘index (as a dimensional criterion for the relaxation) was found in the tissue doppler echocardiographic follow-up. The normalization of the È‘A‘index (initial 0.3975 +/- 0.1106 to 0.705 +/- 0.06 under therapy) was documented significantly (p < 0.05). Conclusions: The addition of ranolazine showed a subjective benefit concerning the reported dyspnoea and angina equivalents in line with the diastolic relaxation disorder. Objectively a relevant amelioration of the tissue doppler ultrasonic parameters was observed. This observation may be important concerning the therapy of hypertensie induced heart failure with diastolic relaxation disorder. Ranolazine inhibits the pathophysiologically increased intracellular sodium influx in late (I Na late) and reduces in this way the calcium overload of the hypertensive cell. Due to this mechanism the calcium effected diastolic left ventricular wallaclampsia will be decreased.