How to short-circuit sudden cardiac death

This unexpected event often occurs before the patient can be hospitalized or admitted to an emergency department. Find out how to prevent it.

Of the 650,000 people in the United States who die of cardiovascular disease (CVD) each year, more than half are felled by sudden cardiac death (SCD), in which the patient expires within an hour of symptom onset. Although these statistics are grim, effective medical management by primary-care clinicians can significantly reduce SCD in high-risk patients.

SCD is caused by electrical problems in the heart—usually ventricular tachycardia or fibrillation—and strikes people of all ages. In children and adolescents, SCD is frequently the result of congenital abnormalities of the cardiac conducting system or of the myocardium. Since SCD is typically the first manifestation of the disorder, these anomalies are rarely detected. Only a small number of these young patients survive an initial episode, and some cardiology experts believe that their siblings should be evaluated preventively.

In adults, more than 80% of SCD events occur in people with CAD. The fatal arrhythmia is often related to acute ischemia or underlying myocardial damage. Most patients at high risk for SCD will already have been diagnosed with CAD. This group includes patients with acute coronary syndrome (ACS), including MI and unstable angina; those who have undergone a revascularization procedure, i.e., angioplasty or coronary artery bypass graft surgery; and those with chronic, stable angina.

While many of the treatments discussed here can also help prevent an initial cardiac event, we will focus on patients at high risk for further cardiac events, including SCD.

A postangioplasty “cocktail”

As primary-care clinicians, we can reduce our high-risk patients’ risk of SCD by managing their medical therapy. An effective strategy involves a “postangioplasty cocktail” that takes into account the following approaches: Dual-antiplatelet therapy. Numerous studies have demonstrated the value of adding clopidogrel (Plavix) 75 mg to aspirin for dual-antiplatelet therapy in patients with ACS. Although this combination can increase the possibility of bleeding, the risk can be minimized by limiting the aspirin dose to 81 mg. In studies to date, most bleeding problems were manageable; although they required transfusion, they were not life-threatening and were apparently gastrointestinal in origin. In addition, bleeding problems almost always resolved in the first few days or weeks and were not a problem in long-term therapy. Recent concern about the long-term safety of drug-eluting stents, with an increase in thrombotic events appearing at about one year and usually after clopidogrel has been stopped, indicates the value of long-term clopidogrel therapy in postangioplasty patients.

Lipid treatment. Statin therapy in CAD patients has been standard for some time, but recent guidelines have begun to recommend much more aggressive treatment. A series of trials comparing various statins and statin doses clearly showed that lower LDL levels are correlated with fewer recurrent cardiac events. Therefore, all high-risk patients should have their LDL lowered to <70 mg/dL, while <100 is the target in all other patients. Therapy with more potent statins, such as rosuvastatin (Crestor) 20-40 mg and atorvastatin (Lipitor) 20-40 mg, will be the cornerstone of treatment, possibly supplemented by ezetimibe (Zetia) 10 mg when the maximum statin dose fails to achieve the LDL goal. Many clinicians are beginning to add niacin or a fibrate to statin therapy to raise HDL or lower triglyceride levels. However, the safety and efficacy of treating HDL or triglycerides in combination with a statin is unproven.

Without specific evidence and without specific goal levels, I have some concern about this approach and do not use it myself. In addition, because of marked drug interactions, gemfibrozil (Lopid, Jezil, and Gen-Fibro) should never be used with a statin.

Beta blockers. Beta blockers have been known for decades to save the lives of heart patients. Optimal doses of a number of popular agents are not entirely clear, and I am concerned that many patients may be underdosed. Extended-release metoprolol (Toprol-XL), soon to be available as the generic, is convenient at once-daily doses of 100-200 mg, but atenolol and immediate-release metoprolol could be given at minimum doses of 50-100 mg b.i.d.

ACE inhibitors. Two long-term studies showed that adding ACE-inhibitor therapy in high-risk patients reduced cardiovascular events and mortality. Each study used a different ACE inhibitor—one used ramipril, the other used perindopril—indicating class effect, but both used the maximum doses. We should titrate the dose, if tolerated, up to the traditional maximum, such as 40 mg for lisinopril or fosinopril.

Heart failure (HF)

Patients with systolic HF are particularly vulnerable to SCD. Several treatments can reduce both the risk of SCD and other cardiac events. Many of these treatments are the same as those discussed above; all have been shown to be effective.

Beta blockers. Two specific beta-blocker regimens have been shown to reduce SCD and other cardiac events in HF patients: carvedilol (Coreg) 25 mg b.i.d. and extended-release metoprolol 100-200 mg daily. These medications should be started at low doses and titrated slowly. No other beta blockers have been shown to be comparable.

ACE inhibitors. Several studies have demonstrated that full-dose ACE inhibitors, as a class, reduce SCD and other cardiac events. As with the beta blockers, ACE inhibitors should be titrated slowly to their full dose.

Candesartan. One study added the angiotensin receptor blocker candesartan (Atacand) to ACE-inhibitor and beta-blocker therapy in HF patients, with a further reduction in cardiac events. This is complicated therapy that needs to be started at a low dose and titrated gradually with close monitoring of both renal function and potassium levels.

Implantable cardiac defibrillator (ICD). In patients with a systolic ejection fraction <30%-35%, the most effective way to reduce the risk of SCD is to use an ICD. Placement of an ICD is now the standard of care in marked systolic HF. We need to evaluate our HF patients’ ejection fractions (usually via echocardiogram) to identify candidates who will benefit from this life-saving therapy.

Dr. Guthrie is professor of emergency medicine at The Ohio State University in Columbus.

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