By Roman Pachulski, MD
There is little more dramatic in its presentation than a patient with cardiac arrest.
Regardless of what field of medicine doctors may practice now, all surely have vivid memories of running to a “code blue” during medical training. As anyone in emergency, cardiac or critical care medicine can attest, the algorithms for treating this catastrophic complication have changed tremendously over the past 25 years. But more fundamentally, we have been striving to preemptively treat high-risk subgroups with the added
benefit of symptomatic improvement
in
heart failure.
It turns out that the road to effective arrhythmia therapy that underlies most cardiac arrests crosses the path of effective heart failure therapy. Although seemingly intuitive now, we followed a bumpy road from frankly counterproductive approaches to effective therapy, and finally preventive interventions.
Eighty eight percent of sudden death is due to cardiac arrhythmia, and of that, 85 percent is due to ventricular tachycardia. It has long been known that survival diminishes about 10 percent per minute after onset of circulatory arrest.
From a public health standpoint, preventive strategies should impact the largest possible number of patients. Unfortunately, as the prevalence of cardiac arrest rises in increasingly high-risk populations from those with prior infarction, to those with heart failure or to those with documented prior ventricular tachycardia, the absolute numbers of patients actually diminishes, robbing the value of prophylactic intervention.
Patients with prior heart attacks have six times the risk of cardiac arrest as the general population, and heart failure patients have nine times the risk.
Early therapeutic attempts were empiric pharmacologic approaches with procainamide, quinidine and fleacainide that under rigorous scrutiny were found to increase mortality. The dated controversy over drug efficacy assessment through invasive electrophysiology study or repeat Holter recordings was thereby rendered moot by the inefficacy of drug therapy.
More recently, in the COMPANION trial even amiodarone had no mortality benefit in the chronic treatment of ventricular tachycardia over optimal pharmacologic heart failure therapy.
A multiplicity of trials including AVID, MADIT 1 and 2, and MUSTT documented the benefit, not only of defibrillation, but prophylactic implantation of a defibrillator in heart failure patients. These large, well-structured trials repeatedly show relative mortality reductions of 20 to 31 percent. Similarly, field trials have documented dramatic survival improvement with early defibrillation using automatic external defibrillators that first responders can operate.
For those office-based primary care practitioners, including many obstetricians who feel they never see cardiac arrest patients, it is worth reviewing that 59 to 64 percent of mildly to moderately symptomatic heart failure patients otherwise well and stable die from cardiac arrest. These constitute the bulk of the office going heart failure patients.
The latest trials, SCD-HEFT and COMPANION investigated the symptomatic benefit of biventricular pacing in heart failure patients with bundle branch block.
Biventricular pacing activates both the right and left ventricle directly rather than activating only the right ventricle and allowing passive activation of the hemodynamically more important left ventricle. Electronic activation of the left ventricle is achieved by cannulating the coronary sinus from the right atrium and placing the lead in a branch vein. Heart failure patients with biventricular pacing live better, and those with defibrillators live longer.
In an analogous fashion, the evolution of heart failure therapy has taken perhaps a counterintuitive turn from digoxin and diuretic to a strong emphasis on afterload reduction, potassium sparing agents and beta blockade.
The only procedural therapy found to improve both the quality and quantity of life in heart failure patients, short of transplant, is biventricular defibrillator implantation.
The gaping maw between heart failure drug therapy and cardiac transplantation with its chronic donor organ paucity and narrow applicability has been bridged by biventricular defibrillator implantation with its diminutive surgical risk in trained hands.
Device implantation results in symptomatic improvement in 80 percent of appropriately selected individuals and can be further improved through the use of advanced echocardiographic techniques including color tissue Doppler mapping to optimize atrioventricular and even interventricular activation times (figures 1 and 2).
The best treatment for cardiac arrest therefore involves the confluence of optimal heart failure pharmacotherapy with beta blockade and biventricular defibrillator implantation when appropriate.
Dr. Roman Pachulski completed his medical training at the University of Ottawa in 1983 and postgraduate training in cardiac electrophysiology at the University of Pennsylvania in 1990. He is board certified and current in Internal Medicine, Cardiology and Cardiac Electrophysio-logy. He currently practices on Stone Oak Parkway in San Antonio, having moved from New York where he was Chief of Cardiology at Bassett Heart Institute, a Columbia University affiliated teaching hospital.
