[Acute viral myocarditis with transient concentric pseudohypertrophy of the left ventricle complicated by cardiogenic shock]. / Miocardite acuta virale con transitoria pseudoipertrofia concentrica del ventricolo sinistro complicata da shock cardiogeno.

The authors report the case of a 38-year-old woman with acute influenza myocarditis, cardiogenic shock and multiorgan injuries. The echocardiogram showed symmetric thickening and severe hypokinesis of the ventricular wall, with a concomitant reduction of the left ventricular cavity due to myocardial edema and cellular infiltration. The myocardial thickening gradually decreased and the ejection fraction improved, as shown by serial echocardiographic evaluations. Blood levels of cardiospecific enzymes were slightly elevated and ECG showed little change. The myocarditis resolved without sequelae. The hemodynamic implications of this transient myocardial thickening and its relationship to steroid therapy are discussed.

Prominent anterior QRS forces: clinical, electrocardiographic and prospective study.

Recent data suggest that the prominent anterior QRS forces (R greater than or equal to S in V1 and/or V2 leads), in the absence of posterior myocardial infarction, right ventricular hypertrophy, or WPW syndrome, are related to an intraventricular conduction disturbance, at times rate-dependent. We followed 240 subjects with prominent anterior QRS forces and without the above mentioned diseases (study group), (mean age: 44.6 +/- 16 years, mean follow-up: 8 +/- 2 years) and 240 subjects without the anterior displacement (control group), (mean age: 44.4 +/- 14 years, mean follow-up: 7.9 +/- 1.9 years). The age distribution, sex, prevalence of organic heart disease, and follow-up period did not show significant differences between the two groups. QRS duration, prevalence of left ventricular hypertrophy pattern, S1 S2 S3 morphology, terminal r wave in AVR and s wave in V6 were similar in the two groups. During the follow-up period the incidence of right and left bundle branch block and fascicular block was very similar in the two groups of patients. These data suggest that prominent anterior QRS forces do not appear to be related to an initial involvement of the main bundle branches and fascicles and do not increase the likelihood of appearance of an intraventricular block of more advanced degree. The clinical, ECG and prospective data are not helpful in localizing either the ventricle or the area of the ventricle affected by conduction disturbance responsible for the anterior displacement. Our data suggest that the prominent anterior QRS forces express a normal variant of ventricular depolarization and that this finding does not have, per se, any unfavourable clinical implication.

Role of the autonomic nervous system in the genesis of first and second degree atrio-ventricular nodal block.

Thirty-four patients with a prolonged A-H interval (group I) and 26 with A-V nodal Wenckebach block (group II) were studied in the basal state and after autonomic blockade (propranolol 0.2 mg kg-1 and atropine 0.04 mg kg-1 in order to assess the role of autonomic system in A-V nodal conduction disturbances. In group I, the A-H intervals did not change significantly after autonomic blockade, whereas pacing cycle length for Wenckebach block, effective and functional refractory periods of the A-V node decreased significantly (P less than 0.05). In the 22 patients with organic heart disease these variables did not change significantly after autonomic blockade, whereas in the 12 without underlying heart disease, they decreased in all cases (P less than 0.001). In the former, the variables of intrinsic A-V nodal conduction were normal in only 9% of patients, whereas in the latter they were normal in 66%. Also in group II, the intrinsic A-H intervals were normal in only 6% of patients with cardiac disease but were normal in 63% without underlying heart disease. These data suggest that in the patients with first and second degree A-V nodal block and organic heart disease, the conduction disturbance is predominantly related to intrinsic involvement of A-V node, whereas in the subjects without underlying heart disease the A-V nodal blocks appear mainly related to autonomic alterations.

Poor R wave progression in pure mitral stenosis. Correlation with hemodynamic data.

Poor R wave progression in the right precordial leads has frequently been reported in patients with pure mitral stenosis, but has never been investigated from clinical and hemodynamic points of view. In this work the clinical, electrocardiographic and hemodynamic data of 19 patients (mean age: 49 +/- 8.6 years), with pure mitral stenosis and poor R wave progression (study group) were compared with those of 19 subjects with pure mitral stenosis and normal R wave progression (control group). The age, sex distribution and duration of mitral valve disease were similar in the two groups; also clinical status, i.e. the distribution in the functional classes (NYHA), was similar in the two groups. Mitral valve area was similar in the two groups (1.3 +/- 0.5 vs 1.1 +/- 0.3 cm2), whereas wedge pressure, mean pulmonary artery pressure, systolic and diastolic right ventricle pressures and total pulmonary resistances showed significant lower values in patients with poor R wave progression compared to those with normal R wave progression (P less than 0.05). The hemodynamic variables of left ventricle and the cardiac index were similar in the two groups. In study group patients there was higher prevalence of vertical axis (P less than 0.05). These data indicate that in pure mitral stenosis, clinical status is similar in patients with poor R wave progression and in those with normal R wave progression, whereas in the former there is slighter hemodynamic involvement of the right ventricle.

Clinical effects of digoxin on sinus node and atrioventricular node function after pharmacologic autonomic blockade.

The effects of digoxin on sinus node and atrioventricular (AV) node function were studied in 18 patients (mean age 53.6 years) with normal intrinsic heart rates. Electrophysiologic testing was performed both during basal state and after autonomic blockade with propranolol and atropine. Full digitalization was achieved by intravenous administration of digoxin (0.02 mg/kg) given in three divided doses over a 24-hour period. The following day, after a basal recording, autonomic blockade was again induced and the study was repeated. During basal state, digoxin significantly prolonged the sinus cycle length (SCL) (p less than 0.01) and the AH interval (p less than 0.01). However, when the intrinsic sinus node functions were compared (i.e., the values obtained after autonomic blockade), digoxin did not produce significant changes in intrinsic SCL, corrected sinus node recovery time, and sinoatrial conduction time. No significant changes were noted even in the intrinsic AH interval and AV nodal refractory periods. These findings suggest that: (1) intravenous administration of digoxin in therapeutic doses does not produce any depression of the intrinsic functions of the sinus node and AV node; and (2) the depressant effects induced by digoxin during basal state appear to be mediated through the autonomic nervous system.

Slight middle slurring in V1-V2 without bundle branch block. An electrocardiographic and follow-up study.

A slight middle slurring in V1 and/or V2 with rS morphology (R less than S) in these leads, without right or left bundle branch block is a nearly ignored electrocardiographic finding. The purpose of this work is to provide a prospective and electrocardiographic analysis of this finding. We followed 200 subjects with middle slurring in V1 and/or V2, in the absence of bundle branch block (study group), (age: 41.5 +/- 19 years, follow-up period: 5.7 +/- 2.5 years) and 200 subjects with rS morphology in V1-V2 without the middle slurring (control group), (age: 39.8 +/- 20 years, follow-up period: 5.2 +/- 2 years). The age, sex, prevalence of organic heart disease, QRS duration and follow-up period did not show significant differences between the two group. In the study group there was a higher prevalence of vertical axis (P less than 0.001), of S1S2S3 morphology (P less than 0.001) and of terminal r wave in a VR (P less than 0.05) compared to control group. During the follow-up period, a right bundle branch block appeared in 19 subjects of study group (incomplete in 15 and complete in 4) and in 2 (complete) of control group (P less than 0.001). A left bundle branch block appeared only in one patient of study group and in one of control group. We conclude that the isolated slight middle slurring in V1-V2 expresses an initial involvement of the right bundle branch system and increases the likelihood of appearance of right bundle branch block.

[Electrophysiologic effects of propafenone in patients with sinus node dysfunction]. / Effetti elettrofisiologici del propafenone in pazienti con disfunzione del nodo sinusale.

The electrophysiologic effects of intravenously administered Propafenon (1,5 mg/kg) were evaluated in 16 patients (mean age: 62,1 +/- 11 years) with sinus node dysfunction, shown by sinus bradycardia or intermittent sino-atrial block. The variations of sinus cycle length were not statistically significant (NS), (1137,1 +/- 244,9 msec versus 1191,9 +/- 321,1 msec). In one patient sinus rate markedly decreased from 36 to 28 beats/min. In 2 patients the cycle length of a junctional rhythm was comparable before and after drug administration; in both patients the rate of the junctional rhythm decreased and in one markedly (from 39 to 32 beats/min). Sinoatrial conduction time increased in 4 patients and decreased in 6. The variations were not statistically significant (223,8 +/- 76 msec versus 230,6 +/- 75,9 msec). In one patient the sinoatrial conduction time which was normal during the control study, could not be evaluated after Propafenon due to the appearance of a retrograde block between the atrium and the sinus node. Maximum corrected sinus node recovery time was prolonged by the drug in 9 patients and shortened in 5. In 2 patients the sinus node recovery time was prolonged to about 10 sec. The mean value of corrected sinus node recovery time increased from 883,6 +/- 995,8 msec to 1820,5 +/- 2894 msec (NS). Propafenon significantly prolonged the effective refractory period and the functional refractory period of the atrium, as well as the A-H, H-V and QRS intervals, the A-V node functional refractory period, the relative refractory period of His-Purkinje system and the ventricular effective refractory period.(ABSTRACT TRUNCATED AT 250 WORDS)