LAUSR

Objective: Heart insufficiency with preserved ejection fraction -HFpEF- (or diastolic Relaxation disorder) is a consequence of left ventricular dysfunction induced by a long-term hypertension. It is observed as well despite effective treatment with antihypertensive drugs. The analysis and quantification of the diastolic relaxation disorder is feasible using tissue-doppler-echocardiography by registration of the E’A’- ratio. Typical clinical symptoms are dyspnea and angina pectoris equivalents. An influence on heart failure with preserved ejection fraction 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. Upon this mechanism the calcium dependent diastolic left ventricular wall tension will be decreased. We hypothesized that ranolazine will improve hypertensive induced diastolic dysfunction through this mechanism. Design and method: We report about 15 patients with essential hypertension (7 male and 8 female, aged 72.7 +/− 9.8 years) with normal renal function (serum creatinine 0.9 +/− 0.2 mg/dl) with exclusion of a macrocoronary induced ischemia, which complained of dyspnoea and/or angina pectoris equivalents under moderate exercise. A coincidental exercise induced hypertension was excluded. Despite efficient continuation of the antihypertensive treatment all these patients showed a diastolic relaxation disorder with normal LV systolic function. After educational advertising ranolazine (375 mg, 2 × d.) was administerd additionally. As a sodium magnesium antiport was described in hypertensive cells earlier, we measured ionized and plasma magnesium before and after treatment, too. Results: During observation time of this study,blood-pressure and heart rate showed no significant changes to values pre-treatment. The patients by themselves reported a subjective amelioration using a standard questionaire. After 10.3 +/− 3.1 days a significant (p < 0.01) decrease of the diastolic relaxation disorder was measured in the control of tissue-doppler-measurement (initial E’A’ ratio = 0.598 +/− 0.131 versus E’A’ ratio under ranolazine treatment with 0.766 +/− 0.179). This normalization of E’A’- index (as a parameter of diastolic relaxation disorder) was observed in all 15 patients. Plasma and ionized magnesium values showed no significant change under ranolazine treatment. Conclusions: The addition of ranolazine in hypertensive heart disease is safe and effective.