Effect of acute myocardial infarction on cholesterol ratios.

OBJECTIVE: In patients with acute myocardial infarctions (MIs), cholesterol levels are no longer valid after 24 h from presentation because acute MI causes a rapid decline in serum levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol. The objective of this study was to evaluate the effect of acute MI on the total cholesterol/HDL cholesterol ratio and the LDL cholesterol/HDL cholesterol ratio. METHODS: The study consisted of 45 patients who were admitted to the hospital with acute MIs. Serum levels of total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides were determined on day 1 post-MI and day 4 post-MI. The total cholesterol/HDL cholesterol ratio and the LDL cholesterol/HDL cholesterol ratio were calculated. Serum lipid levels and cholesterol ratios were compared between day 1 post-MI and day 4 post-MI. RESULTS: From day 1 post-MI to day 4 post-MI, the mean (+/- SD) serum levels of total cholesterol (188.4 +/- 52.5 vs. 170.5 +/- 57.2 mg/dL, respectively; p = 0.01), LDL cholesterol (120.3 +/- 48.9 vs. 105.9 +/- 43.0 mg/dL, respectively; p = 0.009), and HDL cholesterol (45.0 +/- 18.5 vs 39.3 +/- 16.1 mg/dL, respectively; p < 0.001) decreased, but the mean serum level of triglycerides (119.2 +/- 81.2 vs 149.3 +/- 68.3 mg/dL, respectively; p = 0.006) increased. The cholesterol ratios, however, remained unchanged between day 1 post-MI and day 4 post-MI. The total cholesterol/HDL cholesterol ratio was 4.59 +/- 1.84 on day 1 post-MI and 4.67 +/- 1.77 on day 4 post-MI (change not significant). The LDL cholesterol/HDL cholesterol ratio was 2.96 +/- 1.58 on day 1 post-MI and 2.99 +/- 1.44 on day 4 post-MI (change not significant). CONCLUSION: Acute MI does not affect the cholesterol ratios. Therefore, when the absolute levels of serum cholesterol are no longer valid (beyond 24 h after an MI), the cholesterol ratios still could be useful for cholesterol risk assessment in patients with acute MIs.

Prognostic value of serum cardiac troponin I in ambulatory patients with chronic renal failure undergoing long-term hemodialysis: a two-year outcome analysis.

OBJECTIVES: We sought to evaluate the prognostic value of cardiac troponin I (cTnI) in asymptomatic, ambulatory patients with chronic renal failure treated with long-term hemodialysis. BACKGROUND: Smaller, short-term follow-up studies on this subject have given conflicting results. METHODS: A total of 126 ambulatory patients with chronic renal failure treated with long-term hemodialysis were followed for two years for all-cause mortality, cardiac mortality, all-cause hospital admissions and cardiac hospital admissions. Serum cTnI was measured before dialysis at the time of study entry. RESULTS: One hundred two patients had normal serum levels of cTnI (< or =0.03 ng/ml) and 24 patients had elevated levels (0.015 +/- 0.007 vs. 0.053 +/- 0.029 ng/ml, p < 0.0001). No significant difference in all-cause mortality (20 vs. 4 deaths), cardiac mortality (4 vs. 1 death), all-cause hospital admissions (1.74 +/- 1.72 vs. 1.25 +/- 1.19 admissions/patient) or cardiac admissions (0.52 +/- 0.89 vs. 0.33 +/- 0.76 admissions/patient) was present between the patients with normal cTnI levels and those with elevated cTnI levels. Serum cTnI was not significantly different between patients who died versus those who survived (0.022 +/- 0.019 vs. 0.022 +/- 0.021 ng/ml). Serum cTnI was not an independent predictor of all-cause mortality, cardiac mortality, all-cause admissions or cardiac admissions. Age (older) and serum albumin (lower) were independent predictors of all-cause mortality, whereas a history of myocardial infarction was an independent predictor of cardiac mortality. Serum sodium (lower) was an independent predictor of all-cause hospital admissions, whereas hypertension and previous myocardial infarction were independent predictors of cardiac admissions. The best predictors of the time to death were age (older) and serum sodium level (lower), irrespective of the serum cTnI levels. CONCLUSIONS: Cardiac troponin I has a limited role in predicting mortality and hospital admissions in asymptomatic patients with chronic renal failure treated with long-term hemodialysis.

Acute ventricular rate control in atrial fibrillation: IV combination of diltiazem and digoxin vs. IV diltiazem alone.

OBJECTIVE: To analyze the efficacy of an IV combination of diltiazem and digoxin vs IV diltiazem alone for acute ventricular rate control in patients with atrial fibrillation. DESIGN: Prospective, randomized, open-label study. PATIENTS AND METHODS: Fifty-two patients with atrial fibrillation and uncontrolled ventricular rates were randomized to receive either an IV combination of diltiazem and digoxin or IV diltiazem alone and were observed for 12 h. The successful rate control was defined as a ventricular rate < 100 beats per minute (bpm) persisting for 1 h or conversion to sinus rhythm. The loss of rate control was defined as an increase in the ventricular rate to > 100 bpm persistently for > 30 min or rebound to atrial fibrillation. RESULTS: In both treatment arms (n = 26 each), all patients achieved successful and comparable ventricular rate control at 12 h. The mean (+/- SD) time taken to achieve successful rate control was shorter in the combination arm (15 +/- 16 vs. 22 +/- 22 min). Six patients in the combination arm and 11 in the diltiazem-alone arm experienced episodes of loss of rate control. This loss in the combination arm was less than that in the diltiazem-alone arm (14 vs 39 episodes; p = 0.05). The loss of rate control per patient in the combination arm was also less than that in the diltiazem-alone arm (2.0 +/- 1.0 vs. 3.5 +/- 1.9 episodes per patient; p = 0.04). CONCLUSIONS: This study demonstrates that in patients with atrial fibrillation who have a rapid ventricular response, the IV combination of diltiazem and digoxin results in a more efficacious ventricular rate control with fewer fluctuations than that achieved by therapy with IV diltiazem alone.

The comparative effects of drive and test stimulus intensity on myocardial excitability and vulnerability.

The number and intensity of stimuli that set basic cycle length in cardiac electrophysiological studies can influence the electrical properties assessed by extrastimuli. The relative contribution of drive (S1) and test (S2) stimulus intensity in defining myocardial excitability and vulnerability has not been reported. The purpose of this investigation was to assess this interaction and to determine whether atrial and ventricular findings differed. The effects of S1 and S2 intensity on atrial and ventricular stimulus-intensity-refractory-period curves were determined in open-chest dogs: comparisons were made between curves with S1 intensity varied between diastolic threshold (DT) and 10 mA and S2 intensity maintained at DT and those with S1 intensity maintained at DT and S2 intensity varied between DT and 10 mA. S1-S1 was held constant and S1-S2 varied. The effects of different stimulation sites, cycle length, number of stimulations, and neural blockade were assessed. S1 intensity amplification shifted atrial stimulus-intensity-refractory period curves in the direction of increased excitability and vulnerability; the changes were more pronounced than those obtained by modulating S2 intensity. The changes produced by increasing S1 intensity were evident at different cycle lengths and were enhanced by an increased number of stimulations, but were not evident when S1 and S2 were delivered at different atrial sites. Although beta-blockade attenuated the effects of increasing S1 intensity somewhat, the addition of cholinergic blockade virtually abolished it. Ventricular refractoriness was also changed by modulation of S1 intensity, but the changes were less striking. In the atrium, modulation of S1 intensity has greater effects of stimulus-intensity-refractory-period relations than modulation of S2 intensity; in the ventricule, the converse is true.

Verapamil prolongs atrial fibrillation by evoking an intense sympathetic neurohumoral effect.

BACKGROUND: Verapamil is an effective drug to slow ventricular rate in atrial fibrillation (AF). Clinically, however, i.v. verapamil enhances AF despite experimental evidence suggesting favorable effects of the drug on AF-induced electrical remodeling of the atria. METHODS AND RESULTS: To clarify this controversy, i.v. verapamil's effects were determined in 41 anesthetized dogs, including 6 after beta-blockade. Intravenous verapamil (0.20 mg/kg, bolus, and 0.20 mg/kg/h, infusion) increased the duration of AF (induced by a single extrastimulus), from 19 +/- 6 to 130 +/- 24 s, P < 0.001, and slowed its ventricular response, from 246 +/- 25 to 110 +/- 15 min-1, P < 0.001. Mean aortic pressure, P = 0.002, and systemic vascular resistance, P < 0.035, decreased, and mean right atrial pressure increased, P < 0.001. Plasma norepinephrine concentration increased by 502 +/- 83 pg/mL, P < 0.001, plasma epinephrine concentration by 804 +/- 206 pg/mL, P = 0.002, and plasma total catecholamine concentration by 1606 +/- 366 pg/mL, P = 0.001. Prolongation of AF was related to an increase in mean right atrial pressure, R = 0.49, P = 0.014, right atrial wall tension, R = 0.45, P = 0.044, and plasma norepinephrine concentration, R = 0.83, P < 0.001, with plasma norepinephrine concentration remaining as an independent predictor of AF lengthening on multivariable analysis. In the presence of beta-blockade, verapamil produced comparable or more exaggerated hemodynamic effects, but it did not promote AF. CONCLUSION: The prolongation of AF by verapamil can be related directly to the intense sympathetic neurohumoral effect that occurs following the drug's administration.

Influence of prior ACE inhibitor therapy on morbidity and mortality following acute myocardial infarction.

BACKGROUND: Angiotensin-converting enzyme inhibitor (ACE-I) therapy reduces complications of acute myocardial infarction (MI) even when the therapy is started very early after an acute event. This study sought to determine whether administration of ACE-I therapy prior to acute MI is related to subsequent patient morbidity and mortality. METHODS: Chart review of 318 consecutive patients admitted between September 1995 and December 1996 with a diagnosis of acute MI. Outcome data were compared between patient groups receiving ACE-I therapy prior to infarction and those who were not. RESULTS: Sixty-four patients (20%) were receiving prior ACE-I therapy. They experienced smaller MIs, as determined by peak creatine kinase elevation (1066 +/- 134 vs. 1510 +/- 95 IU; p < 0.05), and fewer Q-wave infarctions (p < 0.05) than did patients who were not receiving prior treatment. The severity of coronary artery disease, defined by an angiographic score, was similar for the two groups. Mortality rates, including patients resuscitated from ventricular fibrillation, were similar within the first 72 hours of admission (3% vs. 2%; p = NS), but patients receiving prior ACE-I therapy showed a greater long-term in-hospital mortality rate (14% vs. 5%; p < 0.05) related to more heart failure deaths. Multivariate logistic regression analysis identified age, treatment with digoxin prior to acute MI, and left ventricular ejection fraction after infarction, but not ACE-I therapy taken prior to infarction, as significant independent predictors of mortality and combined morbidity and mortality. CONCLUSIONS: In a group of patients experiencing an acute MI, those receiving prior ACE-I therapy were more likely to sustain fewer transmural MIs and smaller infarcts. Chronic ACE-I therapy may have cardioprotective effects during acute myocardial ischemia.

Specificity of cardiac troponin I and creatine kinase-MB isoenzyme in asymptomatic long-term hemodialysis patients and effect of hemodialysis on these cardiac markers.

OBJECTIVES: The objectives of this study were: (1) to evaluate the specificity of cardiac troponin I and creatine kinase-MB isoenzyme in ambulatory asymptomatic chronic renal failure patients on long-term hemodialysis, and (2) to evaluate the effect of hemodialysis on the serum levels of cardiac troponin I and creatine kinase-MB isoenzyme. METHODS: One hundred and forty-four consecutive ambulatory asymptomatic chronic renal failure patients on hemodialysis for a minimum of 1 year were evaluated clinically. Serum cardiac troponin I and creatine kinase-MB isoenzyme levels were measured with specific monoclonal antibodies before and after dialysis using ACCESS Troponin I and ACCESS CK-MB assays. RESULTS: The specificity of serum cardiac troponin I was 83% with a cutoff level of 0.03 ng/ml, which is an expected level for healthy population, but it rose to 100% with a cutoff level of 0.15 ng/ml, which is a reference level for patients with acute myocardial infarction. Twenty-four (17%) patients had borderline elevation in cardiac troponin I (>0.03 to <0.15 ng/ml). A history of angina pectoris was more common in the borderline-elevated cardiac troponin I subgroup. In 28% of the patients, serum creatine kinase-MB isoenzyme levels were increased with a specificity of 72% at a cutoff level of 4 ng/ml, which is the upper limit of normal, but the specificity rose to 98% by increasing the cutoff level value to 10 ng/ml. There were no statistically significant differences in serum levels of cardiac troponin I and creatine kinase-MB isoenzyme before and after dialysis. CONCLUSIONS: Cardiac troponin I is highly specific in ambulatory asymptomatic chronic renal failure patients on long-term hemodialysis; borderline elevations in cardiac troponin I may represent microinjury to the myocardium. A serum level of creatine kinase-MB isoenzyme >2.5 times of the normal upper limit may be highly specific in this patient population. Hemodialysis per se does not significantly change the serum levels of cardiac troponin I and creatine kinase-MB isoenzyme.