European journal of cardiology最新文献

A 65-yr-old woman presented with severe congestive cardiac failure and physical signs of an atrial septal defect. Investigation by cardiac catheterisation and cross-sectional echocardiography showed a persistent left superior vena cava draining through an enlarged coronary sinus into the right atrium. In addition, the left atrium was connected to the coronary sinus by two defects in its lateral wall. The atrial septum was intact. The physiological result of this rare anatomical abnormality was a large left-to-right shunt with a small right-to-left component. The defects were closed surgically.

In order to study whether wall motion abnormalities detected by two-dimensional (2D) echocardiography can be quantified and correlated with infarct size, we compared wall motion abnormalities viewed by 2D echocardiography in experimental canine infarction with post-mortem infarct size. Nineteen mongrel dogs underwent left anterior descending coronary artery snare occlusion. They were sacrificed 6 h later. Infarct sizing was done by technetium 99-m stannous pyrophosphate scintigraphy of the excised, sliced left ventricles. Fourteen dogs had both 2D echo wall motion abnormalities and infarctions. Four dogs failed to develop infarction and had no or minimal wall motion abnormalities. Inter-observer variation in 2D echocardiographic measurements was small. Wall motion abnormalities correlated with infarct size both in the 14-dog subgroup with infarction (r = 0.75, P less than 0.003) and all the 18 dogs that completed the protocol (r = 0.87, P less than 0.001). Thus, wall motion abnormalities in experimental canine myocardial infraction can be roughly quantified by 2D echocardiography and correlated with post-mortem infarct size measured by scintigraphy.

The pharmacodynamic effects (changes of systolic time intervals, STI, reaction of pulmonary arterial pressure) of digitoxin were studied in 7 patients with severe congestive heart failure in comparison with the corresponding plasma level. STI indicated glycoside-dependent changes, i.e. shortening of LVETc and QS2c and normalization of prolonged PEPc, while ICT shortening was less observed. In 2 patients with cor pulmonale a pulmonary oedema occurred accompanied with prolonged LVETc. During the early period of glycoside-dependent recompensation no significant correlation between STI shortening and glycoside plasma level was observed. Because of the retarded normalization of the haemodynamics of the pulmonary circulation and because of possible side-effects, rapid digitalization has to be reconsidered.

The circumstances attending a fatal or non-fatal recurrence of myocardial infarction have been analysed for participants in the Ontario Multicentre Exercise-Heart Trial. After an average of some 20 mth observations, 51 of the 751 participants had sustained a recurrence (rate 4.07 per 100 participant years). Some 24% of episodes were closely associated with various types of physical activity, and a further 22% noted vigorous exercise (sometimes of an unusual nature) a few hours previously. Exercise-related episodes were associated with poor programme compliance and ST segmental depression during test exercise, but were unrelated to the prescribed regimen (high or low intensity physical activity). Continuing smoking and a history of recent angina were associated with a risk of recurrence; both were seen less commonly with recurrence in high intensity exercisers than in their low intensity exercise counterparts. Exercise-induced ST segmental depression was associated with a higher frequency of fatal recurrences in high than in low intensity exercisers (P less than 0.05); there may thus be a 'high-risk' subgroup for whom vigorous exercise is contraindicated, and the existence of such a group could confound therapeutic trials of exercise-centred rehabilitation.

Electrophysiological measurements were made before and after the intravenous administration of mexiletine in 14 patients with preexcitation syndromes. Following a single infusion of 3 mg/kg body weight plasma concentrations of mexiletine fell rapidly and after 15 min, significant changes in electrophysiological measurements were not found. Higher plasma mexiletine concentrations, bringing about a pharmacological effect, were attained when a second intravenous infusion was also given. The results suggest a minimum effective plasma concentration for mexiletine of about 0.5 mg/l. Side-effects were minimal and their production was largely dependent on the rate of drug infusion. Electrophysiological measurements in previous studies may have been made at a time when plasma mexiletine concentrations were below an effective level and this could explain a disparity in their findings.

Nine hearts from children who died from noncardiac causes were perfused within 3 h of death with 2.5% glutaraldehyde, 0.1 M sodium cacodylate, pH 7.2, at 4 degrees C. Each heart was perfused continuously for 4 h using a perfusion pressure of 110 mm Hg. The ultrastructural characteristics of the perfused atrial and ventricular myocardium and conduction system, including sinoatrial, atrioventricular node and Purkinje fibers, were studied. These observations were compared with standard published observations on similar tissues. The results demonstrate that the present method yields comparable results and hence provides a simple, yet effective, means for studying ultrastructural aspects of the heart and its conduction system in children. In addition, this method permits satisfactory gross morphologic examination of the organ.

To provide further evidence for the participation of the sinus node in so-called sinus node reentry in man, right atrial stimulation and endocardial mapping were performed in a case with sustained tachycardias which met the commonly accepted criteria for sinus node reentry. In addition to right atrial mapping, the activation of the high left atrium was depicted from the right pulmonary artery. The results clearly showed that in this patient the high right atrium was indeed the site of origin of the atrial echo beats which could be elicited by programmed premature atrial stimulation. The high left atrial electrogram (from the right pulmonary artery) was activated 35 msec after the high right atrium thus excluding the possibility of reentry in Bachmann's bundle. Atrial mapping during echo beats revealed a right atrial activation pattern which was similar to that observed during spontaneous sinus rhythm. Sinus node reentrant beats could also be evoked by programmed premature stimulation of the low lateral right atrium. In conclusion, activation of the high right atrium prior to the high left atrium is an important additional criterion for defining sinus node reentry in man. Thus, the recording of the left atrial signals from the right pulmonary artery helps to exclude reentry in the high left atrium, e.g. Bachmann's bundle.

Biplane cineventriculograms of the right ventricle at rest and during exercise were made of 16 patients with a right coronary artery stenosis of greater than 50% and less than 90% to explain the alteration of the volumes and function of the right ventricle during exercise-induced angina pectoris. The right ventricular enddiastolic volume increases from 113 +/- 6.6 ml/m2 to 133.9 +/- 9.8 ml/m2 (P less than 0.001). The endsystolic volume increases from 48.9 +/- 4.1 ml/m2 to 52.9 +/- 5.3 ml/m2. The stroke volume index increases from 64 +/- 5.5 ml/m2 to 81 +/-8.3 ml/m2 (P less than 0.001). At the same time the ejection fraction increases from 56.5 +/- 2.9% to 60.2 +/- 3.2% (P less than 0.05). The left ventricular enddiastolic pressure increases from 12.8 +/- 1.5 mm Hg to 26.6 +/- 1.6 mm Hg (P less than 0.001). The enddiastolic pressure of the right ventricle increases from 5.8 +/- 0.5 to 12.2 +/- 0.8 mm Hg (P less than 0.001). The mean velocity of diameter shortening, VD, increases from 0.9 +/- 0.06 D/s to 1.12 +/- 0.09 D/s (P less than 0.05). Exercise-induced angina pectoris leads to a considerable increase of the left ventricular enddiastolic pressure and therefore to an increase of the right ventricular afterload. The increase of afterload in patients with a right coronary artery stenosis is compensated by a considerable increase of the enddiastolic volume: the pump-function during exercise-induced angina pectoris is maintained by an increase of preload.

In order to elucidate the electrophysiological nature of the short P-R interval we have studied 15 patients with this phenomenon and a normal QRS complex in the electrocardiogram; none of them had a history of arrhythmias. His bundle electrography and atrial stimulation were used to study the conductivity and refractory periods of the atrioventricular (AV) junction. In 13 cases the studies were repeated after the administration of verapamil. Baseline recordings showed a shortened A-H interval in 6 cases, a shortened H-V interval in 6 and in 3 more with a borderline H-V interval. During rapid atrial pacing A-H interval prolongation was abnormal in 10 cases that showed small increases or sudden prolongations at certain atrial rates. The effective nodal refractory period was shorter than normal. A double AV nodal pathway was demonstrated in one patient and another developed junctional reentrant tachycardias at fixed extrasystolic intervals. After verapamil the A-H interval increased in all but one patient. Significant changes were recorded for the AV nodal refractory periods. In the patient with dual AV nodal conduction verapamil prolonged conduction time and refractory periods through both pathways, and in the one with reentrant tachycardias upon atrial stimulation it abolished the tachycardia. In the presence of a normal QRS, a short P-R interval may be due to shortened conduction time through the AV node, and/or the His-Purkinje network. Our observations tend to rule out the presence of a complete bypass of nodal tissue. Despite the absence of a history of arrhythmias these patients may have electrophysiological abnormalities that predispose them to reentrant AV nodal tachycardias.

The contribution of atrial systole in the left ventricular (LV) function and the effects of oral digoxin maintenance therapy on the LV function were evaluated noninvasively in patients who had artificial pacemakers but no clinical manifestation of congestive heart failure (NYHA Class I). Diastolic dimension (Dd), ejection time (ET), and stroke volume were constant in 8 patients without P waves on their electrocardiograms, but in 20 patients with P waves they were variable from beat to beat because of the variation of the PR intervals which caused them to reach their maximum values when the PR intervals were 160 to 200 msec. Ten out of the 28 patients were given 0.25 mg of digoxin daily for 10 days. Dd did not change significantly, but the ET and the systolic dimension were significantly shortened (P < 0.001). Posterior wall excursion, ejection fraction, and mean posterior wall velocity were significantly increased (P < 0.001). It is concluded that (1) atrial contraction is important to the LV function in patients with artificial pacemakers, and (2) that favorable effects on the LV function can be obtained by a small dose of digoxin administered to the patients who had artificial pacemakers but no congestive heart failure.