trandolapril and Hypotension

The presence of hyponatremia has been perceived to increase the risk of adverse events on initiation of treatment with angiotensin-converting enzyme inhibition in heart failure patients. The aim of this study was to investigate if baseline hyponatremia (plasma Na(+) <135 mmol/L) predicts development of hypotension and renal impairment in patients with myocardial infarction (MI) and left ventricular dysfunction (LVD) treated with angiotensin-converting enzyme inhibitors.. A retrospective analysis was performed with data from the Trandolapril Cardiac Evaluation (TRACE) a double-blind randomized study. Plasma sodium levels were available in 1,731 patients, who were considered as the study population. Patients 3-7 days after MI with left LVD (LVEF ≤0.35), were randomized to trandolapril (n = 876) or placebo (n = 873). Baseline hyponatremia did not predict development of hypotension or worsening renal function after 1 month in patients treated with trandolapril compared with placebo (122 ± 19.1 mm Hg vs 123.2 ± 20.4 mm Hg [P = .84]; and creatinine clearance 57.4 ± 21.4 mL/min vs 55.2 ± 21.0 mL/min [P = .8]). There was no interaction between hyponatremia and the effect of trandolapril (P = .68).. Mild hyponatremia was not a contraindication for the initiation of treatment with angiotensin-converting enzyme inhibitors in patients with post-MI heart failure.

Topics: Aged; Aged, 80 and over; Angiotensin-Converting Enzyme Inhibitors; Double-Blind Method; Female; Follow-Up Studies; Humans; Hyponatremia; Hypotension; Indoles; Male; Middle Aged; Prospective Studies; Retrospective Studies; Survival Rate; Treatment Outcome; Ventricular Dysfunction, Left

This is a randomised, double-blind, placebo-controlled, four-way crossover study to determine if indomethacin attenuates the hypotensive effect of trandolapril. Twenty-three hypertensive patients (diastolic blood pressure (DBP) 95-115) requiring NSAID were recruited. Seventeen completed the study. Three week treatment periods: trandolapril 2 mg od and indomethacin 25 mg tds, trandolapril 2 mg and placebo, indomethacin and placebo, placebo and placebo. Clinic and ambulatory BP after 3 weeks of each treatment. Study had 85% power to detect a 5 mm Hg difference in BP (s.d. 7 mm Hg). End of treatment clinic BPs were: 152.9/98 mm Hg (95% CI 147.2, 158.6/95.8, 101.4) with placebo and placebo; 150.4/94.9 mm Hg (95% CI 144.7, 156.1/92.1, 97.7) with trandolapril and indomethacin; 148.2/96.5 mm Hg (95% CI 142.5, 153.9/93.7, 99.3) with trandolapril and placebo; and 156.6/97.4 mm Hg (95% CI 150.9, 162.3/94.6, 100.2) with indomethacin and placebo. There were no significant interactions between trandolapril and indomethacin for clinic systolic BP (SBP) (P = 0.79) or clinic DBP (P = 0.87). When trandolapril treatments (placebo or with indomethacin) were compared to treatments without trandolapril (placebo or indomethacin), trandolapril lowered clinic SBP by 5.4 mm Hg (P = 0.047) and DBP by 2.3 mm Hg (P = 0.08). Mean ambulatory BP was: 140.6/88.2 mm Hg (trandolapril and placebo); 142.8/89.7 mm Hg (trandolapril and indomethacin); 149.6/95.0 mm Hg, (indomethacin and placebo); 147.7/94.0 mm Hg (placebo and placebo). Compared with placebo, trandolapril and placebo lowered BP by 6.5/7.5 mm Hg (P < 0.001, SBP; P < 0.001, DBP). Compared with indomethacin, trandolapril and indomethacin lowered BP by 5.0/5.5 mm Hg (P = 0.001, SBP; P < 0.001, DBP). In the present study trandolapril 2 mg lowered clinic SBP and ambulatory BP, but indomethacin did not attenuate this. Indomethacin had no significant effect on either clinic or ambulatory BP. The antihypertensive effects of trandolapril in this study were modest. Patient selection factors may have contributed to the observed responses, but it seems unlikely from these data that a clinically important drug interaction has occurred.

Topics: Adult; Aged; Angiotensin-Converting Enzyme Inhibitors; Anti-Inflammatory Agents, Non-Steroidal; Blood Pressure; Cross-Over Studies; Double-Blind Method; Drug Interactions; Drug Therapy, Combination; Female; Humans; Hypotension; Indoles; Indomethacin; Male; Middle Aged

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