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The Acute Infarction Ramipril Efficacy (AIRE) trial [17] [25] showed a 27% reduction in mortality for patients receiving ramipril for chronic heart failure following a myocardial infarction. Ramipril was found to have similar results as telmisartan , an angiotensin II receptor blocker .
Medications included in the polypill were atenolol, 100 mg; ramipril, 10 mg; hydrochlorothiazide, 25 mg; and simvastatin, 40 mg. Only 4.4% of those who took the polypill alone had a heart attack, stroke, artery-reopening procedure or died of heart disease, compared to 5.5% who took the placebo.
A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in one of the coronary arteries of the heart, causing infarction (tissue death) to the heart muscle. [1] The most common symptom is retrosternal chest pain or discomfort that classically radiates to the left shoulder, arm, or jaw. [1]
At least 10% of patients with STEMI do not develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subsequent Q waves on EKG after reperfusion therapy. Such a successful restoration of flow to the infarct-related artery during an acute myocardial infarction is known as "aborting" the myocardial infarction.
In India, nifedipine is manufactured by JB Chemicals, and comes in brands Nicardia Retard (Nifedipine 10 mg, 20 mg tablets) and Nicardia XL 30/60, which are Nifedipine Extended Release tablets. [34] In Switzerland, nifedipine is sold only as a generic version of extended release formulation, under the names Nifedipin Mepha and Nifedipin Spirig ...
Fatal and nonfatal myocardial infarction by 36% (P=0.001) Coronary revascularization by 30% (P=0.016). These results were seen in combination therapy with beta blockers, and were found to be safe and effective in improving coronary artery disease outcomes in patients with heart rates of 70 bpm or more. [19]
The duration of action of a single oral dose is longer than the half-life and may be up to 12 hours if the single dose is high enough (e.g., 80 mg). [72] Effective plasma concentrations are between 10 and 100 mg/L. [ citation needed ] Toxic levels are associated with plasma concentrations above 2000 mg/L. [ citation needed ]
The blood pressure lowering effect of molsidomine can be amplified significantly by PDE5 inhibitors, potentially leading to fainting or myocardial infarction, and to a lesser extent by other antihypertensive drugs such as beta blockers, calcium channel blockers, or other nitrovasodilators. Ergolines can antagonise the effects of molsidomine. [2 ...