Acute coronary syndrome: short-term effects of early intravenous metoprolol on maximum P wave duration and P wave dispersion.

In patients with acute coronary syndrome (ACS), the presence of atrial fibrillation (AF) results in worse inpatient outcomes than in those without AF. Two electrocardiographic markers, maximum P wave duration (P(maximum)) and P wave dispersion (P(dispersion)), have been assessed because they reflect conduction abnormalities in patients with paroxysmal AF. b blockers are known to have beneficial effects in patients with ACS. This prospective study was conducted to investigate whether early intravenous (IV) metoprolol injection acutely decreases P(maximum) and P(dispersion) in patients with ACS. This study involved 100 consecutive patients with ACS who were divided into 2 groups according to whether or not they received early IV metoprolol. Group 1 consisted of 19 patients who received IV metoprolol within 3 h after onset of symptoms, and group 2 consisted of 81 patients who did not receive IV metoprolol within 3 h after symptom onset because of late admission. P(maximum) and P(dispersion) were measured on admission and again at 2 h after admission. Two-dimensional echocardiographic examination was also performed. For patients who received early IV metoprolol, P(maximum) and P(dispersion), measured 2 h after admission, were shorter than values at admission (P<.001). Conversely, P(maximum) and P(dispersion), measured 2 h after admission, did not differ significantly from values at admission in patients who did not receive early IV metoprolol (P=.292 and P=.236, respectively). IV administration of metoprolol reduced values for P(maximum) and P(dispersion), measured 2 h after admission, among patients with ACS who were admitted within 3 h after onset of symptoms.

Clinical importance of elevated CK-MB and troponin I levels in congestive heart failure.

Myocyte necrosis has been considered to play a fundamental role in the pathophysiology of congestive heart failure (CHF), which has usually evolved as a consequence of depletion of compensatory mechanisms and contractile reserve of myocardium. Elevated levels of creatine kinase MB (CK-MB) and troponin I (Tn-I) have been regarded as biochemical markers of myocyte necrosis. This study was planned to investigate the specificity and sensitivity of Tn-I and CK-MB in CHF and to examine the correlation of these markers with disease severity. A total of 104 patients (38 female, 66 male; mean age, 66 y [range, 36-89]) with symptoms and signs of heart failure on admission and with a reduced left ventricular ejection fraction (EF; by transthoracic echocardiography) were labeled "the patient group," and 58 patients (40 female,18 male; mean age, 61 y [range, 34-77]) with no signs or symptoms of CHF and with a normal EF detected by transthoracic echocardiography were included in the study as "the control group." Left ventricular EFs, end-diastolic diameters, and end-systolic diameters of patients in both groups were measured. Blood samples were drawn from all patients in both groups on admission, so that levels of CK-MB and Tn-I could be measured. All patients in both groups also underwent coronary angiography. Conditions leading to elevation of CK-MB or Tn-I were considered exclusion criteria. The 2 groups failed to show any significant differences in terms of mean age and the presence of coronary artery disease, hypertension, or diabetes mellitus (P>.05). Mean EF in the patient group was lower than that in the control group (P<.05). Mean CK-MB and Tn-I in the patient group were significantly higher than in the control group (P<.05). In the patient group, hypertensive patients were found to have significantly higher mean values of CK-MB than were seen in normotensive patients in the same group (P<.05). In the patient group, 52 cases were considered to be class I-II (New York Heart Association [NYHA]) (group 1), and 52 were considered to be class III-IV (group 2). Group 1, group 2, and the control group did not differ significantly from one another with regard to the presence of coronary artery disease, hypertension, and diabetes mellitus (P>.05). The mean EF in group 2 was significantly lower than that in group 1 and in the control group (P<.05); the mean EF in group 1 was significantly lower than that in the control group (P<.05). Group 1 values did not differ significantly from those of group 2 or the control group in terms of enzymatic markers (P>.05), but group 2 had significantly higher mean values of CK-MB and Tn-I than were noted in the control group (P<.05). The uphill course of CK-MB and Tn-I values from the control group to group 2 (NYHA class III-IV) was statistically significant (P<.05). Serum concentrations of CK-MB and Tn-I may become elevated in severely symptomatic patients with CHF (particularly NYHA class III-IV), demonstrating a relationship between clinical severity of the disease and elevation of myocardial enzymes (CK-MB and Tn-I).

Tortuosity of coronary arteries: an indicator for impaired left ventricular relaxation?

OBJECTIVE: To investigate the relationship between coronary tortuosity and impaired left ventricular relaxation. METHODS: One hundred and four subjects who underwent coronary angiography were included in the study. Left anterior descending, left circumflex, and right coronary arteries were traced. Tortuosity was identified by the finding of >/=3 bends (defined as >/=45 degrees change in vessel direction) along main trunk of at least one artery. Study population were divided into tortuosity (n = 54) and no tortuosity (n = 50) groups. Subjects were all submitted to pulsed-wave Doppler and two-dimensional echocardiographic examination to assess left ventricular functions. RESULTS: For subjects with tortuosity, early transmitral inflow (E) velocity was lower, late transmitral inflow (A) velocity was higher, E/A ratio was smaller compared with subjects without tortuosity (P < 0.001). Subjects with tortuosity had longer deceleration time of E velocity (DT) and isovolumic relaxation time (IVRT) than did subjects without tortuosity (P < 0.001). End-diastolic interventricular septal and left ventricular posterior wall thicknesses were greater in subjects with tortuosity than those without tortuosity (P = 0.01 and P = 0.005). There was an inverse correlation between total number of arteries with tortuosity and E/A ratio (r = -0.750, P < 0.001). Total number of arteries with tortuosity displayed correlations with DT (r = 0.723, P < 0.001) and IVRT (r = 0.703, P < 0.001). CONCLUSIONS: This study depicts that coronary tortuosity is associated with impaired left ventricular relaxation.Thus, coronary tortuosity might be an indicator of impaired left ventricular relaxation.

Torsades de pointes with a severely prolonged QT interval induced by an initial low dose sotalol intake.

Many drugs, including sotalol, have been implicated in prolonging QT interval and triggering torsades de pointes, a potentially fatal ventricular arrhythmia, especially during chronic therapy or in case of acute high dose toxicity. We report here a case with a severely prolonged QT interval and torsades de pointes after an initial intake of low dose sotalol (80 mg), indicating a probable inherent individual oversensitivity to sotalol.