doi: 10.1093/oxfordjournals.eurheartj.a061545pmid: N/A
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VIITASALO,, M.T.;KALA,, R.;EISALO,, A.
doi: 10.1093/oxfordjournals.eurheartj.a061546pmid: 6705801
Abstract Ambulatory electrocardiographic recordings were obtained from 35 male athletes between 14 and 16 years old, and from 35 male nonathlete controls of the same ages, in order to determine the effects of regular physical training on cardiac electrical activity. In the young athletes, the heart rates were significantly (P<0-01) lower than in the nonathletes. Sinus intervals over 2-00 s were present in five athletes (14%) and one control (3%). First-degree atrioventricular block was detected in eight athletes (23%) and four controls (11%), and second-degree block was detected in seven athletes (20%) and one control (3%) (P<0-05). Ventricular premature beats were present in 60% of athletes and 57% of controls. The bradycardia in athletes did not predispose to ventricular ectopic activity, since heart rates at the times of occurrence of extrasystoles were higher in athletes than in controls. Even after two years of regular physical training there are significant differences in sinus nodal function and atrioventricular conduction as between young athletes and controls. Arrhythmia, electrocardiography, sports medicine This content is only available as a PDF. © 1984 The European Society of Cardiology
ROELANDT,, J.;KLOOTWUK,, P.;LUBSEN,, J.;JANSE, M., J.
doi: 10.1093/oxfordjournals.eurheartj.a061555pmid: 6705808
Abstract Ten instances of sudden cardiac death documented with longterm ambulatory electrocardiography are described. All had coronary artery disease. The lethal arrhythmia was ventricular fibrillation in seven, bradyarrhythmia ending in asystole in two, and electromechanical dissociation in one. There was no specific arrhythmia pattern in the preceding hour of the terminal event and no predictable electrical trigger for the lethal arrhythmia. The literature on the subject has been reviewed. It appears from the information available that larger series of documented sudden death cases are needed if one wishes to define subgroups with a preventable case of sudden cardiac death. Coronary artery disease, Holter monitoring, sudden death, ventricular fibrillation, ventricular asystole This content is only available as a PDF. © 1984 The European Society of Cardiology
WENNERBLOM,, B.;EKSTRÖM,, L.;HOLMBERG,, S.
doi: 10.1093/oxfordjournals.eurheartj.a061547pmid: 6705802
Abstract We have compared the effectiveness of two different mobile coronary care systems with regard to mortality from cardiac arrest (CA) outside hospital in Gothenburg, Sweden. In period 1, the mobile coronary care unit (MCCU) was part of a randomized study of the effect of an MCCU versus standard ambulances on early mortality from ischaemic heart disease. The MCCU was single, hospital based and manned by two CCU nurses and two ambulance drivers. The organization ran on workdays 08.00 a.m. to 17.00p.m. from October, 1973 to May, 1978, corresponding to twelve months of effective lime. One-year data for the MCCU have been calculated by extrapolating to a 100% allocation to the MCCU. In period 2, from November, 1980, through December, 1981, also corresponding to twelve months of effective time, the system was reorganized to a mobile intensive care unit (MICU) manned by paramedics 24 h all days of the week, and part of the time by CCU nurses. The MICU was dispatched to all suspected emergencies and the treatment capacity was defibrillation, endotracheal intubation and, part of the time, drugs. Simultaneously with the MICU, the nearest standard ambulance was dispatched and the first crew to arrive started cardiopulmonary resuscitation (CPR). Comparing the extrapolated data from period 1 with the exact data from period 2, there was an increase in period 2 of dispatches to subjects in CA due to heart disease from 59 to 181. The retrieval of subjects in ventricular fibrillation (VF) increased from 20 to 87 as a result of reduced delay times from the collapse to alarm, start of CPR and defibrillation. The number of patients less than 75 years old, discharged alive from hospital increased from 6 to 19. In subjects retrieved in VF in period 2, 43% survived if CPR was started within 5 min and 7% if CPR was delayed more than 5 min. 56% of the cases received CPR within 5 min and defibrillation within 8 min and 50% of them survived, but if defibrillation was delayed more than 8 min, only 14% survived. In conclusion the reorganization of an MCCU system from a single, hospital based MCCU manned by CCU nurses and ambulance drivers to a decentralized rapid response system with paramedics was associated with an improvement from 6 to 19 survivors, less than 75 years old, in one year. Acute myocardial infarction, resucritation, MCCU, MICU, cardiac arrest This content is only available as a PDF. © 1984 The European Society of Cardiology
PADELETTI,, L.;MICHELUCCI,, A.;FRADELLA,, G.A.;MONIZZI,, D.;FANTINI,, F.
doi: 10.1093/oxfordjournals.eurheartj.a061548pmid: 6705803
Abstract The effects of atropine on sinoatrial conduction time (SACT) measured directly (SACTD)from the sinus node electrogram (SNE) were investigated in 15 patients with normal sinus node function. A comparison was undertaken with the results furnished by indirect methods which employ premature (SACTS) and asynchronous atrial stimulation (SACTN) to calculate SACT. In the control stale SACTD was 92-5±16-4ms. SACTS 78-2±22 ms, and SACTN 97-9±32-2 ms. After atropine SACTD was 70-6±15-6ms (P<0-0O05), SACTS 46-7±14-3ms (P<0-0005) and SACTN 43-1 ±12-7 ms (P<00005). Mean percent decreases of SACTN (51-6 ± 21) and SACTS (37-4±18) were statistically greater than that of SACTD (23-5±13-3) (P<0-0005 and P<001 respectively). While the reduction of SACTS and SACTN was greater than that of sinus cycle length (SCL) (29-2%), SACTD showed a reduction significantly less than that of SCL (P<0-005). Thus, SNE recording confirms that atropine induces a shortening of SACT in normal patients, but significantly less than that indicated by indirect methods. Atropine, Sinus node, Sinoatrial conduction This content is only available as a PDF. © 1984 The European Society of Cardiology
LAIRD-MEETER,, K.;PENN,, O.C.K.M.;HAALEBOS,, M.M.P.;, van DOMBURG, R.;LUBSEN,, J.;BOS,, E.;HUGENHOLTZ,, P.G.
doi: 10.1093/oxfordjournals.eurheartj.a061549pmid: 6608448
Abstract The first 1041 patients who underwent an isolated aorto-coronary bypass operation in the same institution since it opened in 1971, were followed for up to 10 years to determine their prognosis. The mean follow- up time was 3-5 years. The probability of survival at five years was 94 ±2% (95% confidence limits). This was similar to the survival of the general Dutch population matched for age and sex. Multivariate survival analysis with the proportional hazards model did reveal a relationship of the rate of death with sex and age at operation; however this was not significant. There was a trend to a higher death rate with more vascular involvement (rate ratio of 3 vessel-versus 1 vessel disease of 1-9, N.S.) and a significant association with a low ejection fraction (EF) (ratio EF≤)0.30 v. EF ≥0.55 of 2.7. P<0.05). Though surgery seems to eradicate the poor longterm outlook for patients with more serious vascular disease, the adverse influence of decreased left ventricular function on survival is not changed. Aorto-coronary bypass surgery, survival, coronary artery disease, left ventricular function This content is only available as a PDF. © 1984 The European Society of Cardiology
AHO,, K.;GORDIN,, A.;PALOSUO,, T.;PUNSAR,, S.;VALKEILA,, E.;KARVONEN,, M.;INKOVAARA,, J.;PASTERNACK,, A.
doi: 10.1093/oxfordjournals.eurheartj.a061550pmid: 6705804
Abstract The relationship of thyroid autoantibodies and elevated TSH level to indices of cardiovascular diseases was studied in two population series monitored for 5 years and in a cross-sectional hospital series. In a cohort of 1105 males, initially 55-74 years of age, deaths due to cardiovascular causes occurred in 19% of subjects with thyroid autoantibodies and in 11% of controls matched for age (P<0-05). In another cohort of 1045 males and 1223 females, initially 40-64 years of age, no difference emerged in males, while 6 out of 20 females who died of cardiovascular causes had thyroid autoantibodies, compared with 18% in the whole series. In a series of 97 hospital patients with myocardial infarction, 7 patients had thyroid autoantibodies as opposed to 12 antibody-positive subjects among controls matched for age and sex. Elevated TSH level appeared to be no better an indicator of cardiovascular morbidity or mortality than thyroid autoantibodies. It is concluded that thyroid autoimmunity may act as a cardiovascular risk factor under certain circumstances, but it does not have any general significance and the mechanism of action remains unclear. Thyroid autoantibodies, thyrotropin This content is only available as a PDF. © 1984 The European Society of Cardiology
FOUAD, F., M.;EL-TOBGI,, S.;TARAZI,, R.C.;BRAVO,, E.L.;HART,, N.J.;SHIREY,, E.K.;LIM,, J.
doi: 10.1093/oxfordjournals.eurheartj.a061551pmid: 6368232
Abstract In an attempt to study the possible mechanism(s) by which captopril controls resistant heart failure, sequential haemodynamic studies (radioisotope technique) and humoral measurements (plasma renin activity, plasma aldosterone and plasma catecholamines) were obtained in 11 such patients. The studies were made at the time patients became unresponsive to other vasodilators (hydralazine orprazosin); the vasodilator drug was then discontinued and five days later, the ‘no-vasodilator’ studies were obtained. Captopril therapy was then started. Optimum daily maintenance dose of captopril varied from 75 to 200 mg in different patients. Studies were again repeated aftera period of time equal to the duration of the previous vasodilator therapy. Digitalis and diureticdoses were kept constant throughout. Captopril improved effort tolerance in ten patients. Haemodynamically, mean blood pressure and peripheral resistance were lower than during vasodilator therapy (85±3-l v. 92±3-3 mmHgand 47±4-4 v. 59±4-4 U.M2, respectively; p<0-05 for both). Cardiacindex was higher during captopril treatment (l-95±0-15 v. l-63±0-10l/m1, p<0-01) and pulmonary mean transit was normalized by captopril (14-6±l-7 v. 18-4±l-3s, p<0-05). Humoral indices revealed a significant (p<0-05) reduction in plasma aldosterone during captopril therapy (25-9±5-6 ng/dl during captopril, v. 62±22 ng/dl with novasodilators and 50-9±6-l ng/dl with other vasodilators). Moreover, there was a decrease in circulating plasma catecholamines during captopril treatment, but differences between the three treatment periods were not statistically significant. Data suggest that the effectiveness of captopril in controlling congestive heart failure that became resistant to other forms of vasodilator therapy might be related to more than one factor including persistent haemodynamic unloading, decrease of plasma aldosterone, and possibly reduction of sympathetic activity. Captopril, vasodilators, heart failure This content is only available as a PDF. Author notes *This study was supported, in part, by a grand from the Whitaker Foundation and from N1H Grant 6835. © 1984 The European Society of Cardiology
doi: 10.1093/oxfordjournals.eurheartj.a061552pmid: 6705805
Abstract The metabolic activity of platelets in patients with advanced rheumatic heart disease (RHD) was estimated by measurement of heat production in a microcalorimeter. Twenty-nine patients were randomly selected and prospectively followed before and after valve replacement with Bjork-Shiley prosthesis. Before the operation a significantly (P<0-02) elevated platelet heat production wasfound compared with normal subjects, 63 ±5 fW/cell and 59 ±4 fW/cell, respectively, probably due to the presence of a younger and metabolically more active platelet population. Platelet count before the operation was significantly lower than normal (P<0-001).Platelet heat production did not correlate with either type of valvular disease, the presence of valvular calcification or atrial fibrillation. After valve replacement the platelet heat productionsignificantly decreased (P<0-001) to 58±5 fW/cell and the platelet count normalized. The highest incidence of thromboembolic manifestations was in the immediate postoperative period. The greatest reductions in platelet heal production. 19% and 27% were observed in two patients with thromboembolic events, as compared with an average of 4% for therest of the operated patients without complications. The possible relationship between changes in platelet heat production and thromboembolism in patients with RHD is discussed. Platelet counts, platelet metabolism, rheumatic heart disease, prosthetic valves, thromboembolism This content is only available as a PDF. © 1984 The European Society of Cardiology
doi: 10.1093/oxfordjournals.eurheartj.a061553pmid: 6705806
Abstract Reflux of contrast into the inferior vena cava and hepatic veins during held expiration was studied in 70 subjects using subxiphoid 2D echocardiography. Venous reflux of contrast occurred in 7<19 normal sub jects (group 1), 13<17 patients with definite or probable tricuspid regurgitation (group 2), 10<13 patients with congestive cardiac failure (group 3) and 10<21 patients with miscellaneous cardiac conditions unlikely to be associated with tricuspid regurgitation (group 4). There were 30 patients with no appearance of microbubbles in the inferior vena cava and hepatic veins on suspended expiration: 10 of these had reflux of contrast when breathing was restarted. Of the 17 patients with atrialfibrillation, 14 showed reflux, but there were 3 patients with no reflux. We conclude that the appearance of contrast in the IVC and hepatic veins may be found in many subjects in whom tricuspid regurgitation is unlikely on clinical grounds, even when recordings are taken in held expiration. Atrial fibrillation alone does not necessarily cause venous reflux of contrast. Demonstration of simple venous reflux of contrast by 2D echocardiography is too non-specific for routine use in the detection of tricuspid regurgitation. Cross-sectional [2D] echocardiography, Contrast Studies, Tricuspid Regurgitation This content is only available as a PDF. © 1984 The European Society of Cardiology
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