Atenolol heart failure with

The ACC/AHA recommends that P-blockers be initiated in all patients with NYHA FC I to IV or ACC/AHA stages B through D heart failure if clinically stable.1 To date, only three p-blockers have been shown to reduce mortality in systolic HF, including the selective prantagonists bisoprolol and metoprolol succinate, and the non-selective pr, p2-, and arantagonist carvedilol.29 33 The positive findings should not be extrapolated to be indicative of a class effect, as bucindolol did not exhibit a beneficial effect on mortality when studied for HF, and there is limited information with propranolol and atenolol. 

Propranolol was the first blocker shown to be effective in hypertension and ischemic heart disease. Propranolol has now been largely replaced by cardioselective blockers such as metoprolol and atenolol. All B-adrenoceptor-blocking agents are useful for lowering blood pressure in mild to moderate hypertension. In severe hypertension, blockers are especially useful in preventing the reflex tachycardia that often results from treatment with direct vasodilators. Beta blockers have been shown to reduce mortality after a myocardial infarction and some also reduce mortality in patients with heart failure they are particularly advantageous for treating hypertension in patients with these conditions (see Chapter 13). 

The efficacy of p-AR blockade appears to be superior in achieving reverse remodeling and this is more directly dose-related than that of ACE inhibitors (Frigerio and Roubina 2005). Recently, in a clinical trial examining the effects of metoprolol and atenolol, it was found that patients with heart failure treated with metoprolol... 

A randomized comparison of oral atenolol and bisoprolol in 334 patients with acute myocardial infarction was associated with drug withdrawal in 70 patients (21%) because of significant bradydysrhythmias, hypotension, heart failure, and abnormal atrioventricular conduction (40). Logistic regression analysis suggested that critical events were more likely to occur in patients who were pretreated with dihydropyridine calcium antagonists. 

The SHEP was a landmark double-blind, placebo-controlled trial that evaluated active treatment (chlorthalidone-based, with atenolol or reserpine as add-on therapy) for isolated systolic hypertension. A 36% reduction in total stroke, a 27% reduction in coronary artery disease, and 55% reduction in heart failure were demonstrated versus placebo. The Systolic Hypertension-Europe (Syst-Eur) was another placebo-controlled trial that evaluated treatment with a long-acting dihydropyridine CCB. Treatment resulted in a 42% reduction in stroke, 26% reduction in coronary artery disease, and 29% reduction in heart failure. Similar findings were observed in a Chinese population with isolated systolic hypertension. These data clearly demonstrate reductions in cardiovascular morbidity and mortality in older patients with isolated systolic hypertension, especially with thiazide diuretics and long-acting dihydropyridine CCBs. 

C. Toxicity Cardiovascular adverse effects, which are extensions of the beta blockade induced by these agents, include bradycardia, atrioventricular blockade, and congestive heart failure. Patients with airway disease may suffer severe asthma attacks. Premonitory symptoms of hypoglycemia from insulin overdosage, eg, tachycardia, tremor, and anxiety, may be masked, and mobilization of glucose from the liver may be impaired. CNS adverse effects include sedation, fatigue, and sleep alterations. Atenolol, nadolol, and several other less lipid-soluble beta-blockers are claimed to have less marked CNS action because they do not enter the CNS as readily as other members of this group. 

Atenolol 100 mg daily has been shown to increase the serum disopyramide steady-state levels from 3.46 to 4.25 micrograms/mL and reduce the clearance of disopyramide by 16% in healthy subjects and patients with ischaemic heart disease. None of the subjects developed any adverse reactions or symptoms of heart failure, apart from one of the subjects who had transient frrst degree heart block. ... 

Other case reports and studies describe heart failure, dyspnoea, - sinus arrest, heart block, "" hypotension, " and bradycar-(jj 4,5,8,io,ii,i4-i8 jjj patients taking verapamil with alprenolol, atenolol, metoprolol, " propranolof " or pindolol. In two further cases, bradycardia occurred in patients taking verapamil and using timolol eye drops. Another case has been reported, but this was complicated by the presence of flecainide , (p.844). A number of reports noted that patients experiencing this interaction had reasonable left ventricular function. Heart block and hypotension or cardiogenic shock has also been reported after verapamil was given with atenolol or propranolol in overdose. 

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