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

In situ calibration of fura-2 and BCECF fluorescence in adult rat ventricular myocytes

Quantitation of Ca+ and H+ activities within cells using presently available fluorescent probes is optimal when the fluorescence signal is calibrated in situ after each experiment. Fura-2 and 2',7'-bis(2-carboxy-ethyl)-5,6-carboxyfluoroscein (BCECF) are difficult to calibrate in freshly dissociated adult cardiac myocytes because calibration procedures produce cellular hypercontracture. In situ calibration was accomplished in rat ventricular cells by saturating fura-2 with La3+, an agent known to produce myocardial relaxation. Since fura-2 has different spectral properties when complexed with La3+ than with Ca2+, scaling factors were defined in vitro and then verified by experiments in cultured neonatal myocytes. In adult rat myocytes using the La3+ method, intracellular Ca2+ concentration ([Ca2+]i) was 131 +/- 47 nM (n = 14) in quiescent cells; diastolic [Ca2+]i and systolic [Ca2+]i in myocytes stimulated at 1 Hz were 140 +/- 56 and 1,088 +/- 211 nM (n = 5), respectively. BCECF fluorescence was calibrated in situ by a method that prevented cellular hypercontracture and reported a pH value of 7.10 +/- 0.10 in cells stimulated at 1.5 Hz. An additional advantage of both methods is that the buffers employed prevented large changes in the redox state of intracellular pyridine nucleotides, thus preventing a change in cellular autofluorescence during the calibration procedure

Role of cation gradients in hypercontracture of myocytes during simulated ischemia and reperfusion

We examined the relationship between transsarcolemmal cation gradients and hypercontracture of cardiac myocytes in ischemia and reperfusion using adult rat ventricular myocytes superfused with buffer mimicking normal or ischemic extracellular fluid. Contractile performance of electrically stimulated cells was recorded by an optical video system simultaneously with measurements of intracellular Ca2+ concentration ([Ca2+]i) using fura-2 or intracellular pH (pHi) using 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. While cells were exposed to simulated ischemia buffer, the transsarcolemmal H+ gradient was abolished, [Ca2+]i transient stopped, and twitch contraction of myocytes ceased. Upon reperfusion with normal buffer, H+ gradient was quickly restored, Ca2+ transients restarted with transient increase in systolic Ca2+, and twitch contraction restarted with development of hypercontracture, which continued after [Ca2+]i returned to preischemic level even in the presence of near-normal concentrations of high-energy phosphates. When the transsarcolemmal proton, Na+, and Ca2+ gradients were altered so that Na+ entry via Na(+)-H+ exchange and Ca2+ entry via Ca(2+)-Na+ exchange were made less favorable, the transient systolic overshoot of Ca2+ at reperfusion and development of hypercontracture was largely avoided. These results suggest that Na+ and then Ca2+ entry via the Na(+)-H+ and Na(+)-Ca2+ exchangers, respectively, probably contribute to the increase in [Ca2+]i and hypercontracture of myocytes at time of reperfusion in this model