Cardiac Abnormalities After Aneurysmal Subarachnoid Hemorrhage: Effects of β-Blockers and Angiotensin-Converting Enzyme Inhibitors

Myocardial abnormalities such as cardiac arrhythmias, electrocardiographic (ECG) changes, and neurogenic stunned myocardium have been commonly reported in patients with aneurysmal subarachnoid hemorrhages (aSAHs).1–4 Additionally, the average patient in whom such cardiac anomalies develop is relatively young and otherwise healthy.5 Stimulation of the sympathetic nervous system, in an attempt to maintain tissue perfusion and oxygenation to the brain, results in the release of catecholamines, which function to stimulate heart rate and cardiac contractility and regulate vascular tone.6 Excess catecholamine release from sympathetic and adrenal medullary activation has been posited for the development of central nervous system–mediated myocar-dial injury.7,8 In patients with aSAH, this adrenergic release results in overstimulation of the sympathetic nervous system, essentially increasing systemic vascular resistance and causing afterload stress of the heart. The inability of the heart to contract effectively against this resistance contributes to heart failure and an even further imbalance between oxygen supply and demand.6 In response to the decreased cardiac output by the heart, and subsequent renal perfusion, there is also an increase in renin release by the kidneys, leading to activation of angiotensin II, and excessive vasoconstriction. The culmination of these myocardial events may worsen outcomes after aSAH.9,10 Therapeutic interventions that block these pathways intuitively should be beneficial for aSAH patients by counteracting or reducing these adverse responses. β-adrenergic blockers are indicated for use in the treatment of hypertension, angina pectoris, and cardiac arrhythmias. Therapeutic effects of these medications are achieved by blocking β-adrenergic receptors in the heart to minimize the influence of the sympathetic nervous system, resulting in vasodilatation, and thereby decreasing cardiac workload and oxygen consumption.11,12 β-Adrenergic receptors are also responsible for the release of renin from the kidneys. This mechanism is also blocked through β-blocker therapy, leading to a decrease in blood pressure. Angiotensin-converting enzyme (ACE) inhibitors are indicated in the treatment of hypertension and to reduce the risk of myocardial infarction, stroke, and death in patients with cardiovascular abnormalities. These inhibitors have been associated with improved survival after myocardial infarction. ACE inhibitors function by preventing the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. The inhibition of this conversion leads to decreased peripheral arterial resistance, ultimately resulting in decreased blood pressure. The mechanisms of both the sympathetic nervous system and the renin-angiotensin-aldosterone system can be prevented through the therapeutic effects of β-blockers and ACE inhibitors.13 In patients with aSAH, development of cardiac complications has been attributed to increased sympathetic stimulation, most frequently reported within hours to days after aneurysm rupture.1–4 Because the therapeutic effect of ACE inhibitors and β-blockers is to minimize the influence of the sympathetic nervous system, the purpose of this analysis of patients with acute aSAH was to (1) evaluate the relationship between preexisting cardiac disease and the development of cardiac complications after injury: elevated cardiac enzyme levels (troponin, creatine phosphokinase-MB [CPKMB] index), ECG changes (12-lead ECG and 24-hour Holter monitor), echocardiographic changes, and pulmonary edema and (2) examine the relationship between the reported use of prehospital β-blockers and ACE inhibitors and the incidence of cardiac complications after aSAH.