Non-arrhythmia Group Research Articles

Corrected right ventricular end-diastolic volume and initial distribution volume of glucose correlate with cardiac output after cardiac surgery

Appropriate adjustment of cardiac preload is essential to maintain cardiac output (CO), especially in patients after cardiac surgery. This study was intended to determine whether index of right ventricular end-diastolic volume (RVEDVI), corrected RVEDVI using ejection fraction (cRVEDVI), index of initial distribution volume of glucose (IDVGI), or cardiac filling pressures are correlated with cardiac index (CI) following cardiac surgery in the presence or absence of arrhythmias. Eighty-six consecutive cardiac surgical patients were studied. Patients were divided into two groups: the non-arrhythmia (NA) group (n = 72) and the arrhythmia (A) group (n = 14). Three sets of measurements were performed: on admission to the ICU and daily on the first 2 postoperative days. The relationship between each cardiac preload variable and cardiac index (CI) was evaluated. A p value less than 0.05 indicated statistically significant differences. Each studied variable was not different between the two groups immediately after admission to the ICU. cRVEDVI had a linear correlation with CI in both group (NA group: r = 0.67, n = 216, p < 0.001; A group: r = 0.77, n = 42, p < 0.001), but RVEDVI had a poor correlation with CI (NA group: r = 0.27, n = 216, p < 0.001; A group: r = 0.19, n = 42, p = 0.036). IDVGI had a linear correlation with CI (NA group: r = 0.49, n = 216, p < 0.001; A group: r = 0.61, n = 42, p < 0.001), Cardiac filling pressures had no correlation with CI. Our results demonstrated that cRVEDVI and IDVGI were correlated with CI in the presence or absence of arrhythmias. cRVEDVI and IDVGI have potential as indirect cardiac preload markers following cardiac surgery.

Early postoperative arrhythmias after pediatric cardiac surgery

Early postoperative arrhythmias are a known complication of cardiac surgery; however, little data exists specific to pediatrics. The purpose of this study was to determine the incidence and risk factors associated with the development of arrhythmias immediately after surgery in a pediatric population. Data were collected in a prospective observational format from pediatric patients undergoing cardiac surgery between September 2000 and May 2003. This format included age, anatomy, surgical repair, and serum magnesium and calcium levels, as well as cardiopulmonary bypass and aortic crossclamp times. Patients were continuously monitored, and hemodynamically significant arrhythmias were recorded. Arrhythmias occurred in 28 of the 189 patients enrolled (15%) including 16 with junctional ectopic tachycardia, 7 with complete atrioventricular block, 4 with ventricular tachycardia, and 1 with re-entrant supraventricular tachycardia. Significant differences were found between the arrhythmia and nonarrhythmia groups with regard to age (22 vs 45 months), cardiopulmonary bypass time (189 vs 109 minutes), and aortic crossclamp time (105 vs 44 minutes); P < .05. Magnesium and calcium levels were not significantly different between the groups. Two repairs carried an increased risk: complete atrioventricular septal defect repair, 8 of 11 patients (72%), and the arterial switch 5 of 8 patients (62.5%); P < .05. Atrioventricular septal defects had an even higher incidence when controlled for age, bypass time, and crossclamp time (odds ratio = 7.65). Hemodynamically significant postoperative arrhythmias are a frequent complication of pediatric cardiac surgery. Younger age and longer bypass and crossclamp times are risk factors for arrhythmia. In addition, the repair of atrioventricular septal defects carries an independent risk of arrhythmias.

ECG changes and cardiac arrhythmias in chronic renal failure patients on hemodialysis

Serial 12-lead electrocardiogram (ECG) recordings and 24-hour Holter monitoring were carried out in 39 patients with chronic renal failure, starting just before a routine dialysis session. In an attempt to identify risk factors for cardiac arrhythmias, the results obtained from each patient were correlated with a variety of clinical, hematological, and biochemical data. All patients exhibited ECG changes, which were most pronounced during the first 2 hours of dialysis. The most frequent of these changes were a decrease in T wave amplitude and increase in Tmax time (all patients), an increase of QRS amplitude (61% of patients), shortened or prolonged QTc interval (61%) and ischemic-like ST-T changes (22% and 39%, respectively). Potentially clinically significant arrhythmias occurred in 12 patients (31%) of which 8 were supraventricular, 3 were combined ventricular and supraventricular, and 1 was pure ventricular. The only clinically identified risk factor for complex ventricular and supraventricular arrhythmia was advanced age. The arrhythmia and nonarrhythmia groups differed significantly in their predialysis hematocrit, O 2 content, serum urea, and osmolarity, and in their postdialysis serum phosphorus and osmolarity. The results indicate that patients with chronic renal failure frequently exhibit ECG changes and a high incidence of ventricular and supraventricular arrhythmias, which may be prognostically significant, during and after hemodialysis.

The effect of coenzyme Q 10 on reperfusion injury in canine myocardium

The mechanism of mitochondrial damage during reperfusion injury of ischemic myocardium was studied using mongrel dogs in vivo and isolated mitochondria in vitro. Seventy-seven adult dogs were divided into three groups: the control group (n = 38), the Coenzyme Q10 (CoQ10)-5 mg group (n = 24), and the CoQ10-15 mg group (n = 15). In the control group, the left anterior descending coronary artery (LAD) of the dog was occluded for 15 min followed by 5 min of reperfusion after 40 min of premedication with physiological saline. In both CoQ10 groups, 5 mg/kg or 15 mg/kg of CoQ10 was infused intravenously for 20 min and then physiological saline was administered for 20 min before 15 min occlusion of the LAD. Subsequently, reperfusion was allowed for 5 min. Each group was further divided into two subgroups depending on the presence (arrhythmia group) or the absence (non-arrhythmia group) of ventricular arrhythmias. Immediately after 15 min occlusion, myocardial samples were taken from the normal and reperfused areas to measure CoQ10 content of myocardium. Heart mitochondria were prepared after 5 min of reperfusion from both areas. Arrhythmias appeared in 12 of 38 dogs in the control group (32%), two of 24 dogs in the CoQ10-5 mg group (8%) and none of 15 dogs in the CoQ10-15 mg group (0%). Premedication with CoQ10 increased tissue CoQ10 content in a dose-dependent manner. In the CoQ10-5 mg group, the increase in CoQ10 content of dogs with reperfusion arrhythmias was relatively less than that of dogs without reperfusion arrhythmias. In each group, mitochondrial function was decreased in the arrhythmia group compared to that of the non-arrhythmia group. The increase in free fatty acid (FFA) content and the decrease in phospholipid content were also observed in mitochondria from the reperfused area of each arrhythmia group. The increase in FFA and mitochondrial dysfunction were induced by the incubation of mitochondria in vitro with phospholipase (PLase) A2 or PLase C, and protected by the addition of CoQ10. These results suggest that PLase plays an important role in the development of mitochondrial damage associated with reperfusion.

The effect of verapamil on reperfusion arrhythmia in canine heart.

This study was designed to clarify the mechanism of reperfusion arrhythmia and with the effect of verapamil on arrhythmia. In vivo study: Fifty anesthetized dogs were divided into two groups the control group (n = 37) and the verapamil group (n = 13). The left anterior descending coronary artery (LAD) was occluded for 15 min and then reperfused for 5 min. Physiological saline or verapamil (0.4 mg/kg) was infused 5 min prior to the LAD reperfusion. Eleven (30%) of the control dogs developed "reperfusion arrhythmia" (arrhythmia group) but 26 did not (non-arrhythmia group), while in the verapamil group, none of the 13 dogs developed arrhythmia. Immediately after 5 min reperfusion, myocardial plasma membrane and mitochondria were prepared from the normal and the reperfused area. In the arrhythmia group, an increase in free fatty acids (FFA) and a decrease in phospholipids were observed in membrane samples, and the content of calcium in the mitochondria increased in the reperfused myocardium; these changes were not observed in the non-arrhythmia group or the verapamil group. In vitro study: In vitro study consisted of two experiments. In experiment 1, incubation of myocardial plasma membrane with phospholipase (PLase) A2 increased only the unsaturated FFA, while PLase C increased all the detected FFA. In experiment 2, the effects on myocardial membrane potentials induced by PLase A2 and PLase C were studied by using microelectrodes. Each PLase caused a decrease in the resting potential and in the magitude and duration of the action potential.(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of ventricular tachycardia in patients with ventricular aneurysms: results of intraoperative epicardial and endocardial mapping.

We performed epicardial and endocardial mapping in 11 patients with ventricular aneurysms; six had chronic, recurrent ventricular tachycardia and five had no ventricular arrhythmias more severe than isolated ventricular premature complexes. Forty to 66 epicardial and 16-40 endocardial points were recorded during stable sinus rhythm in each patient. Local electrograms were evaluated as to timing and presence of fragmentation (duration greater than 50 msec, amplitude less than 1 mV, absence of discrete intrinsicoid deflection). Activation of the epicardial surface of the aneurysm was abnormal in all patients, and extended beyond completion of the QRS in three patients in the arrhythmia group and two in the nonarrhythmia group (NS). Activation of the epicardial border zone was normal in all patients. Electrograms from the endocardial surface of the aneurysm were abnormally fragmented in all patients and the mean duration of activation was not different between patients with and without arrhythmias (85.5 +/- 14.1 vs 96.2 +/- 13.8 msec, NS). However, in patients with ventricular tachycardia, electrograms from 33-58.3% (mean 45.5 +/- 8.8%) of the endocardial border zone showed fragmentation, compared with 0-16.7% (mean 4.9 +/- 7.4%) of the endocardial border zone in patients without arrhythmias (p less than 0.05). Fragmentation was always along the septal border of the aneurysm. The mean duration of the most prolonged endocardial border zone electrogram was 97.5 +/- 17.0 msec in ventricular tachycardia patients and 67.0 +/- 27.1 msec in patients without arrhythmia (p less than 0.05). Five of six ventricular tachycardia patients had electrical activity in the endocardial border zone extending beyond the end of the QRS, compared with one of five patients without ventricular tachycardia (p less than 0.05). We conclude that fragmented electrical activity is present in all patients with ventricular aneurysms, but the extent and severity of fragmentation in the endocardial border zone is greatest in patients with recurrent ventricular tachycardia.