Non-Q Wave Myocardial Infarction

Non-Q wave myocardial infarction is a distinct and changing clinical entity characterized by lower initial mortality and a higher rate of reinfarction compared to Q wave infarction. Clinical and pathologic data suggest that the syndrome results from transient or incomplete coronary occlusion resulting in an infarct which is smaller than when Q waves are present. High-risk patients can be identified during hospitalization, allowing for aggressive therapy aimed at revascularization. Relatively few clinical trials have examined initial therapy or secondary prevention in this group of patients. These studies are reviewed and management guidelines suggested

The independent association of renal dysfunction and arrhythmias in critically ill patients

Study objectives: The purpose of this study was to quantify the impact of baseline renal dysfunction on incidence and occurrence of cardiac arrhythmias in the coronary ICU. Background: Renal dysfunction is an established predictor of all-cause mortality in the ICU setting. We set out to evaluate the independent contributory effect of renal dysfunction to arrhythmias and mortality in this population. Design and setting: We analyzed a prospective coronary care unit registry of 12, 648 admissions by 9, 557 patients over 8 years at a single, tertiary center. An admission serum creatinine level was available for 9, 544 patients. Those patients not receiving long-term dialysis were classified into quartiles of corrected creatinine clearance with cutpoints of 46.2 mL/min/72 kg (group 1), 63.1 mL/min/72 kg, and 81.5 mL/min/72 kg. Dialysis patients (n = 527) were considered as a fifth comparison group (group 5). Measurements and results: Baseline characteristics including older age, African-American race, diabetes, hypertension, history of previous coronary disease, and heart failure were incrementally more common with increasing renal dysfunction strata. There were graded, independent increased risks for accelerated idioventricular rhythm (relative risk [RR], 2.43; 95% confidence interval [CI], 1.40 to 4.20; p = 0.002), sustained ventricular tachycardia (RR, 2.07; 95% CI, 1.02 to 4.22; p = 0.04), ventricular fibrillation (RR, 2.42; 95% CI, 1.13 to 5.15; p = 0.02), and complete heart block (RR, 3.64; 95% CI, 1.77 to 7.48; p = 0.0004, group 5 vs group 1). Conclusions: We conclude that baseline renal function is a powerful, independent predictor of cardiac arrhythmias in the coronary ICU population

Intravenous Nitroglycerin for Acute Myocardial Infarction

Intravenous nitroglycerin (IV TNG) has been increasingly used in the setting of acute myocardial infarction. The seven randomized trials comparing IV TNG with placebo, and one trial comparing IV isosorbide dinitrate with furosemide, were reviewed for evidence of beneficial clinical effects. IV TNG in low dosage is safe in the setting of acute myocardial infarction and modestly effective in relieving chest pain. Favorable hemodynamic effects are most pronounced in patients with congestive heart failure. Limited evidence suggests that IV TNG, particularly when administered early, reduces both infarct size and mortality when given prophylactically

Role of antiarrhythmic agents after myocardial infarction with special reference to the EMIAT and CAMIAT trials of amiodarone

The role of antiarrhythmic agents in the post-MI patients has been investigated for several years. Recently, clinical trials have assessed the effects of amiodarone in the post-MI population. The Basel Antiarrhythmic Study of Infarct Survival (BASIS) trial showed a reduction in total mortality, sudden death, and life-threatening ventricular arrhythmias with amiodarone therapy. The European Myocardial Infarct Amiodarone Trial (EMIAT) did not show a mortality benefit, but amiodarone was associated with fewer antiarrhythmic deaths. The Canadian Amiodarone Myocardial Infarction Trial (CAMIAT) showed no significant impact on mortality, but arrhythmia deaths and resuscitated cardiac deaths were reduced. Amiodarone therapy after MI should be reserved for the treatment of symptomatic or sustained ventricular arrhythmias. The current data do not support routine use of amiodarone in all patients after MI

Hypothesis: Paroxetine, a G Protein-Coupled Receptor Kinase 2 (GRK2) Inhibitor Reduces Morbidity and Mortality in Patients With Heart Failure.

The hypothesis that paroxetine decreases morbidity and mortality in patients with heart failure (HF) is plausible but unproven. Basic research demonstrates that inhibition of G protein-coupled receptor kinase 2 (GRK2) both in vitro and in vivo in the myocardium may be beneficial. G protein-coupled receptor kinase 2 antagonism is purported to exert cardioprotective effects immediately following myocardial injury by blunting toxic overstimulation on a recently injured heart. In addition, chronic overexpression of GRK2 inhibits catecholamine induction of vital positive chronotropic and ionotropic effects required to preserve cardiac output leading to worsening of congestive HF. In cardiac-specific GRK2 conditional knockout mice, there is significant improvement in left ventricular wall thickness, left ventricular end-diastolic diameter (LVEDD), and ejection fraction (EF) compared to controls. Paroxetine is a selective serotonin reuptake inhibitor which was recently shown to have the ability to directly inhibit GRK2 both in vitro and in vivo. At physiologic temperatures, paroxetine inhibits GRK2-dependent phosphorylation of an activated G-protein-coupled receptor with a half maximal inhibitory concentration of 35 micromoles, a substantially greater affinity than for other G protein-coupled receptor kinases. In a randomized trial in mice with systolic HF and depressed EF postmyocardial infarction, those treated with paroxetine had a 30% increase in EF, improved contractility, and LVEDD and wall thickness compared to those treated with medical therapy alone. While further basic research may continue to elucidate plausible mechanisms of benefit and observational studies will contribute important relevant information, large scale randomized trials designed a priori to do so are necessary to test the hypothesis