trandolapril and Cerebral-Infarction

A 86-year-old man was referred as he developed a ventricular escape rhythm and severe hypotension. Although external cardiac pacing was begun, the patient subsequently needed intubation as of progressive cerebral deterioration. It turned out that the patient had been treated with a combination compound including hydrochlorothiazide 50 mg, amilorid 5 mg and timolol 20 mg daily for several years. A second combination compound including verapamil 180 mg and trandolapril 2 mg daily was added 5 days prior to hospitalisation due to insufficient control of arterial hypertension.. At admission, the patient was comatose without focal neurological findings. Laboratory analysis revealed lactic acidosis and severe hyperkalemia. No evidence for acute coronary syndrome was found.. Hyperkalemia was successfully treated using calcium gluconate, insulin and glucose. External heart pacing and circulatory support using epinephrine were ceased after conversion into a stable sinus rhythm. Renal failure however did not resolve. CT-scans of the brain were performed on the third day as of protracted coma. They showed extended infarction in the area of the left arteria cerebri media with beginning brain edema. Although mechanical ventilation could be stopped as of sufficient respiration, the patient died on the sixth day.. The presented case describes probably drug-associated severe hyperkalemia and bradycardic arrhythmia, hypotension and (eventually preexisting) normuric renal failure.

Topics: Aged; Aged, 80 and over; Amiloride; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Calcium Channel Blockers; Cerebral Infarction; Diuretics; Drug Combinations; Humans; Hydrochlorothiazide; Hypertension; Hypotension; Indoles; Male; Polypharmacy; Sodium Chloride Symporter Inhibitors; Timolol; Tomography, X-Ray Computed; Verapamil

In this study, we investigated whether angiotensin-converting enzyme (ACE) is involved in the progression of cerebral infarct lesions after middle cerebral artery (MCA) occlusion in rats. After placebo or trandolapril was administered orally for 7 days, we infarcted in the territory of the right MCA by extracranial vascular occlusion and studied the effect of trandolapril on brain ACE activity and infarct size 7 days after MCA occlusion. In placebo-treated rats, brain ACE activity in the infarct side was increased by a significant 1.34-fold compared with that in the non-infarct side 7 days after MCA occlusion. Brain ACE activities in the infarct sides were suppressed to 39.8% by trandolapril treatment. The ratios of unilateral infarcts to the total coronal sectional areas in placebo- and trandolapril-treated rats were 48.1 +/- 3.3% and 37.4 +/- 2.3%, respectively, and the difference between these values was significant. These results demonstrate that inhibition of the increased brain ACE activity in infarct lesions can reduce the infarction area after MCA occlusion.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Arterial Occlusive Diseases; Blood Pressure; Brain; Cerebral Arteries; Cerebral Infarction; Indoles; Male; Peptidyl-Dipeptidase A; Rats; Rats, Inbred WKY; Reference Values; Systole