European journal of cardiology最新文献

A mild mental stress was applied on 39 normal people and on 33 patients with coronary artery disease. The test consisted in their selecting the proper switch out of 2, in order to switch off a lamp out of 3 as soon as possible after its ignition. The 3 lamps were lit by the examiner in a stereotyped random sequence. No consequences were implied against the subjects in case of failure and this was clearly explained to them. The response time of the people was recorded together with their electrocardiogram in a one-channel recorder using a suitable circuitry. The study showed that the response time became progressively shorter during the test only in the coronary group, although the mean value did not differ significantly from that in the normal group. The R-R interval was shortened in both groups but in the coronary group significantly more so than in the normal group. Pretreatment with diazepam reversed both responses of the coronary group. Pretreatment with propranolol mitigated the tachycardiac effect of the test in the coronary group, reversed its effect in the normal group and shortened the response time significantly in the normal group. The objective time measurements by the device used might suggest that in patients with coronary artery disease both the specific (response time) and the nonspecific (R-R interval) behaviour in response to a mental stress differ from that in normal people. This behaviour may be modified by medicaments like diazepam and propranolol.

Amiodarone, 600 mg orally daily, was used in an attempt to control supraventricular tachyarrhythmias in a patient with the sick sinus syndrome. Twenty days from the onset of therapy the Q-T interval lengthened. Episodes of ventricular flutter, ventricular fibrillation and self-terminating ventricular tachyarrhythmia (torsade de pointes) developed on the 28th day of amiodarone therapy. Temporary cardiac pacing prevented further episodes of ventricular fibrillation. Despite the suggestion that this drug may be given in large doses for long periods of time since it has a wide safety margin, we feel that the risk of lethal arrhythmias is such that caution is required in its use.

The echocardiographic study of a patient with a malfunctioning porcine valve in the mitral position is presented. Echocardiography of the mitral valve revealed multiple, dense heterogeneous echoes behind and within the valve stent which were suggestive of vegetations. At the aortic valve level, a clear systolic echo in the left atrium was recorded. This echo probably represented the prolapsing anterior valve stent and was caused by a major dehiscence of the valve stent due to endocarditis.

Symptomatic arrhythmias often occur intermittently in patients with sinus node dysfunction. A diagnostic test with ability to reveal latent sinus disease has therefore been much sought for. Determinations of sinus node recovery time (SNRT) and corrected sinus node recovery time (CSNRT) have been attempted but limitations in their diagnostic power are well recognized. To eliminate a possible masking effect of autonomous neural tone, propranolol 0.1 mg/kg and atropine 0.02 mg/kg was administered to 30 patients with established symptomatic sinus bradydysrhythmias (SSBD) and to a control group of 18 age-matched healthy volunteers. In addition the same procedure was applied to 9 patients with symptoms suggesting SSBD in whom, however, this cause was later excluded. The upper normal limit of CSNRT defined by the control group was 545 msec before and 505 msec after drugs. In the SSBD group, CSNRT was falsely negative in 8 of the 30 patients. Repeated testing after drug inhibition reduced this number to 2 patients. Thus, the sensitivity increased from 73% to 93%. CSNRT determinations were normal in the non-SSBD patients, specificity remaining at 100%. Thus, the discriminative power of electrophysiologic testing for sinus node disease was found to be high when CSNRT determinations were performed both before and after drug inhibition of autonomous neural tone.

Left ventricular systolic pressure (LVSP) and stress in the outer layers of the left ventricular wall were directly recorded in 10 anaesthetised, open-chested dogs. Left ventricular oxygen consumption (VO2) was calculated from the difference in oxygen content in the arterial and in the coronary sinus blood and from the left ventricular coronary flow (LVCF). LVCF was measured in the shunt between the carotid artery and left coronary artery (2 experiments) or in the shunt between the coronary sinus and jugular vein. Tension-time index was calculated either as the product of the mean LVSP and time (TTI(P)), or as the product of mean systolic stress and time (TTI(sigma)). Both TTIs were changed within the broad range by means of exsanguination and blood infusion. Contractility was changed by means of Inderal or noradrenaline infusion. In all experimental conditions VO2/100 g/stroke correlated linearly (P less than 0.01) with TTI(sigma), with correlation coefficient r greater than 0.8. When TTI(P) was used, correlation coefficient r was less than 0.6 and no correlation was found in one series of experiments with noradrenaline infusion. It is concluded that TTI calculated from the directly measured wall stress is a very good correlate of the VO2, which is not the case when the 'classical' TTI is used.

The purpose of this study was to determine a simple and reliable procedure of estimating acute myocardial infarct (AMI) size by measuring serum creatine kinase MB (CK-MB) in few daily blood samples. In 13 patients with AMI blood samples were drawn every second hour for 60 h for determination of serum CK-MB activity. Infarct size was calculated using the CK-MB values of all samples and compared to the size calculated according to various models based on enzyme levels in few samples. Two models, using 3 daily samples, showed very high correlations and satisfactory standard errors of estimate when compared to the infarct size calculated from all samples. One of the 2 models was based on a computerized log-normal curve fit programme and one on accumulation of serum activities of CK-MB. The coefficient of variation of infarct size estimated from thrice-daily sampling was 7.4 and 9.4 for the 2 models. Considering the twenty-fold variation in infarct size a satisfactory quantitation is achieved from 3 daily samples.

Oxygen uptake and cardiac output at rest and during exercise were studied in 19 men operated on for coarctation of the aorta during childhood. Their aerobic capacity and their maximal values for cardiac output, stroke volume and arteriovenous oxygen difference were normal. No differences were found regarding these variables between hypertensive and normotensive subjects. Thus, there was no sign of failure of the left ventricle even in patients with high blood pressure during exercise. Whether the normal arteriovenous oxygen difference indicates a normal distribution of the cardiac output cannot be settled from the present data.

Twenty-three patients with ostium-secundum atrial septal defect (ASD) were studied in order to investigate the etiology of angiographic mitral valve prolapse associated with ostium-secundum ASD. 12 patients (52%) had angiograhic MVP. Ventricular volumes, ejection fraction, segmentary contractility and oxygen step-up were analyzed in all patients. Patients with MVP had smaller enddiastolic and stroke volumes (73 +/- 21.8 ml/m2 and 46.6 +/- 18 ml/beat/m2) than patients without MVP (106.6 +/- 22 ml/m2 and 78 +/- 11.3 ml/beat/m2) (P less than 0.01). Oxygen step-up was greater in patients with MVP (P less than 0.05). No consistent differences in ejection fraction and segmentary contractility were found. Our findings suggest that angiographic MVP associated with ostium-secundum ASD is a functional disorder due to reduced left ventricular enddiastolic volume secondary to the atrial shunt.

In order to study the effects of contrast media on myocardial metabolism the percentage of lactic acid extraction during left ventricular angiography has been determined in 16 normal patients (Group I), and in 29 patients with coronary artery disease (Group II). In addition, the lactic acid uptake was evaluated after atrial pacing (in 10 patients of Group I and in 13 patients of Group II) and after aortography (in 6 patients of Group I and in 9 patients of Group II). Normal patients usually did not show a myocardial lactic acid production after left ventriculography while the patients with coronary artery disease showed a net lactic acid production in the coronary sinus, which was similar to that obtained after atrial pacing stimulation and after aortography. These results indicate that ventriculography can be a useful technique to assess the kinetics of lactic acid uptake or release into the coronary sinus in patients with coronary artery disease and, in this respect could be useful for studying myocardial metabolism in aortic valve disease and to assess the toxicity of different contrast media.

In 1961--1962 five families including 53 members with a familial form of cardiomyopathy (CMP) were examined. Fifteen years later a reinvestigation of the previously examined families was carried out using community registers; mortality as well as new family members were registered. Another 50 family members were thereby added. Three out of 6 young subjects who were diagnosed as having definite (2) or suspected (1) CMP at the initial examination died during the follow-up period. Four of the five families, totalling 39/41 members, were given a thorough noninvasive clinical examination including ECG, phonocardiogram exercise test, measurement of systolic time intervals and carotid arterial pulse curves, and echocardiography (Echo). A high number (17/39) of suspected or definite pathologic echocardiographic changes consistent with CMP was observed on reinvestigation. Eleven of these 17 were asymptomatic. Except for Echo, the non-invasive methods used in this study did not contribute to the diagnosis of CMP, but the non-Echo methods confirmed the Echo findings in those patients with symptoms of cardiac disease. The four reexamined families revealed a very heterogenous pattern of CMP, with both symmetric and asymmetric hypertrophy (ratio symmetric/asymmetric = 15 : 2). It may be questioned whether asymptomatic subjects with borderline changes, indicative of symmetric hypertrophy, will develop definite symmetric CMP or whether their symptoms constitute an early stage of asymmetric CMP. Echocardiographic findings may well fit with the theory of a dominant mode of inheritance.