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UNLABELLED: Extrasystoles (RVES) from the right ventricular outflow tract (RVOT) are a common arrhythmia in routine ECGs. METHODS: In this prospective study 56 consecutive patients with RVES (22 males, 34 females) were examined for morphological and/or functional right ventricular (RV) abnormalities by 12-lead, Holter, exercise ECGs, transthoracic echocardiography and signal averaging. The follow-up time was 3.1-15.8 years (arithmetic mean +/- SD = 7.2 +/- 1.6 years; median, 6.9 years). Patients with hyperthyroidism, structural cardiovascular and/or lung diseases were excluded. RESULTS: A total of 57.1% of the patients with RVES presented with echomorphologic abnormalities of the right ventricle (RV). In 26.8% the echomorphologic right ventricular abnormalities progressed in 33.3% of patients with normal RVs at baseline (group I) and in 21.9% of those with abnormal RVs at baseline (group II). No significant differences were found between the 2 patient groups in terms of age at onset, family history, ECG changes, late potentials and malignant right ventricular outflow tract arrhythmias on 24-h and exercise ECGs. While females predominated in group I, males were numerous in group II (p = 0.006). Sustained ventricular tachycardia, syncope or sudden death were absent throughout the follow-up. CONCLUSION: Patients with RVES carry a good prognosis in terms of morbidity and mortality no matter whether echomorphologic abnormalities are present or not.

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OBJECTIVE: Severe ischemic injury in the first few hours following primary revascularization necessitates acute reoperation. To study the effect of emergency coronary artery bypass grafting, we followed 18 patients for up to 8 years, relating their changes of global and regional myocardial function during the acute event and after secondary revascularization to final outcome. METHODS: A total of 16 patients with coronary artery bypass grafting (CABG) and 2 PTCA were treated for coronary heart disease between 1989 and 1993 and experienced life-threatening ischemic events (94% cardiogenic shock, 39% ventricular fibrillation, 67% ischemic electrocardiograph (ECG) changes) within 2.3+/-1.6 h after primary revascularization. Reoperation was carried out 1.0+/-1.3 h after the occurrence of acute ischemia. Serial echoes were obtained during the acute event and after reoperation as well as during the follow-up period. RESULTS: Of the 18 patients, 8 are currently alive, 5 died within 30 days and 4 within the 1st year. There was one late death 5 years after surgery. Global and regional wall motion was evaluated using short axis views of transesophageal echoes taken during the acute event and after secondary revascularization, and compared with transthoracic echoes in long-term survivors up to 5 years after surgery. During the acute event left ventricular ejection fraction (LVEF) was reduced in 83% of the patients and improved significantly after reoperation (chi2 = 11.74, df= 2, P < 0.01). As to regional wall motion, 50% of the segments in non-revascularized areas remained abnormal. Regional wall motion after reoperation was significantly better in the surviving patients compared with patients dying in the post-operative course (chi2 = 6.23, df= 1, P < 0.05). The revascularization score ( > 75%) of abnormal contracting segments during the acute ischemic event was a significant determinant for long-term survival. CONCLUSION: We conclude that patient outcome is determined by the severity of regional wall motion abnormality during the acute ischemic event, the aggressiveness of the attempt to revascularize these perfusion territories and their improvement after revision. Long-term survival reflects, therefore, the extent of emergency revascularization and therefore the ability to identify ischemic perfusion territories for surgical strategy planning.

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Aims of the study: The evaluation of significant perioperative ischemic processes after coronary artery bypass grafting from postoperative ECG, creatine kinase (CK) and CK iso-enzyme MB remains unreliable and, hence, insufficient. Additional, early available biochemical markers could improve the diagnostics of ischemia. Methods: In 86 patients with multiple vessel disease, activity of serum CK and CK-MB as well as mass of CK-MB, myoglobin and troponin-T were analyzed before and after surgery. Twelve-lead electrocardiograms were evaluated before surgery, 3h postoperatively, and before discharge from hospital. Results: In patients with signs of perioperative ischemia in the 3-hour ECG, primary postoperative peak values of myoglobin and CK were distinctly higher than in patients without signs of ischemia, with median values of 1437 ng/ml vs. 986 ng/ml for myoglobin and of 632 U/l vs. 481 U/l (n.s.) for CK. Sensitivity and specificity of myoglobin were 64 % and 69 %, followed by CK with 61 % and 62 %, respectively. Conclusions: Myoglobin, indicating the risk of perioperative ischemia approximately 45 minutes after declamping of the aorta, is suggested as a candidate for early available routine monitoring.

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The effect of three cardioplegic protocols on perioperative myocardial injury was studied in 62 coronary artery bypass grafting (CABG) patients randomized into three groups with either antegrade or retrograde cold blood cardioplegia, or coronary sinus occlusion during antegrade supply. During the aortic cross-clamp time anterior and posterior septal temperatures were recorded, indicating the distribution of cardioplegic solution within the myocardium. Serum creatine kinase (CK), CK-isoenzyme MB and myoglobin as well as 12-lead electrocardiograms (ECG) were analyzed. Statistical analysis showed no effect of the cardioplegic protocol, whereas the patient's preoperative status, aortic cross-clamp time and intraoperative myocardial temperature had significant (P < 0.05) effects on immediate postoperative CK and CK-MB enzyme release. Creatine kinase-MB peak values were significantly increased in patients with major vessel disease and reduced left ventricular function (92 +/- 53 U/l versus 67 +/- 25 U/l). Both CK and CK-MB values were significantly higher in patients with aortic cross-clamp times of more than 1 h than in patients with shorter clamping times (661 +/- 188 and 78 +/- 40 U/l versus 500 +/- 200 and 57 +/- 24 U/l). Patients with 22 +/- 3 degrees C myocardial temperature before terminal cardioplegia had significantly elevated CK as compared to patients with temperatures of 15 +/- 2 degrees C (665 +/- 185 U/l versus 510 +/- 211 U/l). However, enzyme peak values had only poor predictive power for postoperative ECG changes, suggesting that enzyme peaks were not necessarily a sign of perioperative ischemia. Patients with major vessel disease and reduced myocardial function, with aortic cross-clamp time of more than 1 h and/or inadequate intraoperative myocardial cooling may be highly susceptible to global ischemia and operative procedures, and therefore show elevated peak enzyme levels shortly after surgery. In contrast, elevated myoglobin peaks within 1 h after aortic declamping were significantly correlated to perioperative signs of transient ischemia (P < 0.02).

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The direct and noradrenaline-modulating effects of neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) on venous smooth muscle were studied in healthy volunteers employing the dorsal hand vein compliance technique. Local infusions of NPY had no measurable effect on venous tone, but coinfusion of a constant high dose of NPY (242 pmol/min) with noradrenaline caused a 2.9-fold increase in the mean ED50 for noradrenaline. The dilating effect of VIP on preconstricted hand veins was weak, maximal venodilation could not be achieved, because systemic side effects occurred at submaximally venodilating doses. Coinfusion of noradrenaline with a weakly venodilating, constant dose of VIP (93.2 pmol/min) caused a 0.5-fold decrease in the sensitivity for noradrenaline. Although functional interactions between NPY or VIP and noradrenaline could be demonstrated, the dosages of the peptides required were high. Thus our results indicate that neither NPY nor VIP exert a major direct or noradrenaline-modulating effect on human veins.

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Based on previous experimental and epidemiologic findings, we hypothesized that 17 beta-estradiol (E2) could decrease the alpha-adrenergic responsiveness in venous smooth muscle cells (VSMC), thereby decreasing venous tone and contributing to the pathogenesis of varicose veins. To test this hypothesis, the effect of an acute increase in E2 serum concentrations on venous alpha-adrenergic responsiveness to norepinephrine (NE) was studied in young healthy men. We conducted a double-blind, randomized, placebo-controlled cross-over study in 23 male volunteers; 96 +/- 2 h after a single intramuscular (i.m.) injection of 10 mg estradiol valerate or placebo, we quantified the pharmacologic effects of estradiol on alpha-adrenergic responsiveness of superficial hand veins by venous compliance technique (VCT) and on resting blood pressure (BP). After administration of estradiol, E2 serum levels increased 9.97 +/- 7.54-fold (mean +/- 1 SD, p < 0.001) to within the range of premenopausal preovulatory women. No significant difference was observed in mean dose of NE required for half-maximal venoconstriction (ED50, p = 0.224), however, or in the maximal effect of NE (Emax, p = 0.796) after administration of E2 as compared with placebo. A significant difference in diastolic BP (DBP) (p = 0.039) was observed after E2 administration (64.6 +/- 7.7 mm Hg) as compared with placebo (68.3 +/- 7.6 mm Hg); BP (SBP) was not affected (p = 0.786). Our findings do not support the concept that E2 reduces alpha-adrenoceptor responsiveness of SMC in superficial veins.

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