ABSTRACT
A 64-year-old woman presented to the hospital with a complaint of dyspnea on effort. The 12lead electrocardiogram showed a baseline complete left bundle-branch block, in which the right bundle developed >2:1 block. The subsequent blocked sinus impulse resulted in a ventricular pause that caused the ventricular escape presenting as a QRS complex with right bundle-branch block pattern. However, some of them disclosed typical fusion beats and led to interference dissociation. Although other possibilities including Lenegre's disease or myocardial disease were not excluded, the effective refractory period of both bundle branches degenerated by myocardial ischemia might be attributed to this rhythm.
Subject(s)
Bundle-Branch Block/diagnosis , Bundle-Branch Block/physiopathology , Electrocardiography , Myocardial Ischemia/diagnosis , Myocardial Ischemia/physiopathology , Diagnosis, Differential , Female , Humans , Middle AgedABSTRACT
BACKGROUND: Changes in the plasma adenosine concentration and the effects on left ventricular (LV) function and remodeling in patients with acute myocardial infarction (AMI) remain unclear. MethodsâandâResults: In 58 patients with AMI and 14 subjects without cardiac disease (controls), we measured the plasma adenosine concentration by LC-MS/MS. Blood samples were taken from the antecubital vein on days 0, 1, 7, and 14 after AMI, and from the controls on admission. Cardiac echocardiography was performed in the acute (within 7 days) and chronic (6 months) phases of AMI. There were no significant differences in the plasma adenosine concentrations among days 0 (211.5±150.2 nmol/L), 1 (192.7±141.3 nmol/L), 7 (218.8±154.1 nmol/L), and the controls (136.0±50.9 nmol/L). The plasma adenosine concentration increased significantly on day 14 (321.1±195.4 nmol/L) after AMI as compared with days 0, 1 and 7. AMI patients with a greater increase in the plasma adenosine concentration in the subacute phase showed an attenuation of LV dilation in the chronic phase. The plasma adenosine concentration in the acute phase did not affect the LV ejection fraction in the chronic phase. CONCLUSIONS: The plasma adenosine concentration significantly increased 14 days after AMI, which may contribute to attenuation of LV dilation in the chronic phase.
Subject(s)
Adenosine/blood , Dilatation , Myocardial Infarction/physiopathology , Ventricular Function, Left/drug effects , Ventricular Remodeling/drug effects , Aged , Case-Control Studies , Female , Humans , Male , Middle Aged , Stroke Volume , Time FactorsABSTRACT
BACKGROUND: The role of endogenous adenosine in cardiac patients is still unclear, so we investigated the relationship between the plasma adenosine concentration and left ventricular (LV) function, LV dilation and LV wall thinning in cardiac patients.MethodsâandâResults:In 97 cardiac patients, with angina pectoris, old myocardial infarction, dilated or hypertrophic cardiomyopathy, and valvular heart disease, plasma adenosine concentrations were measured using the LC-MS/MS system, and the LV function, LV end-diastolic dimension (LVDd), LV posterior wall thickness (LVPWth), and interventricular septum thickness (IVSth) were assessed by echocardiography. The plasma adenosine concentration was significantly higher in patients with a LV ejection fraction (EF), an indicator of the LV systolic function, <47% compared with those with LVEF ≥47% (P=0.027). There was no difference between the plasma adenosine concentration and E/e', an indicator of LV diastolic function. The plasma adenosine concentration was significantly higher in patients with LVDd ≥50 mm than in those with LVDd <50 mm (P=0.030). The plasma adenosine concentration was inversely correlated with IVSth (P=0.003) and LVPWth (P=0.0007). The plasma adenosine concentration was significantly higher in patients with IVSth <8 mm than in those with IVSth ≥8 mm (P=0.015), and was significantly higher in patients with LVPWth <8 mm than in those with LVPWth ≥8 mm (P=0.020). CONCLUSIONS: Endogenous adenosine may be related to LV dysfunction, dilation, and wall thinning in cardiac patients.
