Echocardiographic evaluation of right heart responses to sublingual nifedipine in dilated cardiomyopathy.

Twelve patients with dilated cardiomyopathy were studied in order to evaluate whether the favourable effect of Nifedipine on the right heart is due to a direct action of the drug on pulmonary resistances or is related to an improvement of left ventricular function. Echocardiographic examination of left and right heart was performed at basic conditions, after Nifedipine treatment--20 mg sublingually--and after 20 minutes of oxygen breathing (FiO2 75%). This was done in order to verify if oxygen vasodilating action could potentiate the Nifedipine effect. Echocardiographic date were obtained in basic conditions, 10, 20 and 30 minutes after Nifedipine and immediately after oxygen breathing. Ten normal subjects were used for comparison for basic data. Peak Nifedipine activity was observed 10 minutes after administration. At this time inferior vena cava emptying index and systolic pulsation were significantly increased, whereas left and right ventricle isometric contraction time, left and right ventricle ejection time, left and right ventricle isovolumetric relaxation time, end-diastolic left ventricular diameter, inferior vena cava diameters and systolic blood pressure had decreased, thus showing the favourable effect of Nifedipine of both heart sides. Heart rate did not significantly change. Oxygen inhalation induced a significant decrease of right ventricular isovolumetric relaxation and an increase of the inferior vena cava indexes, suggesting an improvement in right heart function, without any change in other parameters. No significant difference was found between data after-oxygen and data obtained 10' after Nifedipine, showing that the Nifedipine effect was not potentiated by oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiographic evaluation of inferior vena cava wall motion and pulmonary flow velocity responses to sublingual nifedipine.

Echocardiographic and cardiac catheterization were used to test the effect of Nifedipine, sublingually administered, on the right heart function and pulmonary flow velocity and pressure in 25 cases. Systolic and mean pulmonary pressure, wedge pressure, mean right atrial and ventricular end-diastolic pressure, aortic pressure, and total pulmonary resistance decreased after Nifedipine in 10 patients who underwent diagnostic cardiac catheterization. While pulmonary flow velocity, expressed as the slope of the contrast echo lines on the pulmonary valve, increased as a mean value after Nifedipine, it showed different behaviour in single cases and thus failed to provide any reliable conclusion as to the effect of Nifedipine. Nifedipine slightly reduced the internal diameters of the inferior vena cava and significantly increased the values of collapsibility and emptying indexes and pulsation. The results confirm the beneficial effect of Nifedipine on right heart function and pulmonary bed. In addition, echocardiography is seen to be a valuable and reliable non-invasive means of testing the acute and chronic effects of either Nifedipine or other drugs on the right heart sections.

Contrast echocardiographic features of pulmonary hypertension and regurgitation.

Linear contrast echo configuration on the pulmonary valve M-mode echogram was assessed in 28 patients with pulmonary hypertension, in 10 with pulmonary regurgitation, and in 10 normal subjects. Contrast echo parallel lines filling the total systolic phase of the pulmonary valve were recorded in normal subjects. Contrast echo lines stopping in early systole around the pulmonary valve mid-systolic notch were seen in all the patients with pulmonary hypertension in relation to changes with the pulmonary flow. Contrast echo lines reversing the early diastole and crossing the pulmonary valve echogram during diastole were detected in all the patients with pulmonary regurgitation, consistent with the reversed flow across the valve. The use of contrast echocardiography to diagnose both pulmonary hypertension and regurgitation may provide further useful information, particularly when the orientation and time of appearance of the contrast echo lines are related to the systolic and/or diastolic phases of the pulmonary valve M-mode echogram.

Subxiphoid echocardiographic assessment of left ventricular wall in old myocardial infarction.

We studied by cineangiography and standard and subxiphoid echocardiography the left ventricular wall motion in 50 patients with old myocardial infarction and 10 normal subjects. Coronary artery angiography showed a good correlation with the electrocardiographic site of infarction and with the asynergic areas detected by cineventriculographic examination and bidimensional echocardiography. From the correlation of data related to the asynergic areas detected by angiographic and echocardiographic methods it was possible to establish that subxiphoid approach allows to visualize the posterior-lateral wall whereas the parasternal approach the posterior-inferior wall of the left ventricle. Two-dimensional echocardiography from the subxiphoid approach resulted to be a useful and reliable technique for detecting the apical asynergies. The left ventricular wall motion parameters detected by M-mode echocardiography showed significant modifications in all the groups either in the comparison SUBX versus ST or in that with the control group. The subxiphoid approach either M-mode or bidimensional was, therefore, useful in the evaluation of the asynergic areas of the left ventricular lateral wall. The association of SUBX with ST provides further information on the left ventricular wall motion and then, since different areas are visualized with the two techniques, on the extent of myocardial damage.

[Electrophysiological evaluation of ventricular tachycardia by right and left ventricle endocardial mapping (author's transl)]. / Rilievi elettrofisiologici nelle tachicardie ventricolari con il mappaggio endoventricolare destro e sinistro.

Eight patients with ventricular tachycardia (VT) have been studied by unipolar recordings of 7 endocardial points of the left ventricle (LV) and 6 endocardial points of the right ventricle (RV) in order to record if possible: 1) where the VT arose; 2) a continuous electrical activity during the sistodiastolic phase of the intracardiac ECG [late potentials (LP)], suggesting the reciprocating mechanism of VT. All the patients underwent cardiac catheterization with left and/or right ventriculography. A coronary arteriography was performed in four cases. Four patients had no evidence of heart disease; one patient had aortic stenosis; one patient had two vessels coronary disease and extensive ipo-akinesis of the LV; two patients had dyskinetic areas of the RV. In all the cases it was possible to identify where the VT arose by means of recordings during spontaneous VT episodes (the sites of origin of the VTs were stated in the points where the intracardiac QRS began with an intrinsic deflection), or by means of asyncronous ventricular stimulation (the sites of origin of the VTs were stated in the points where the ventricular stimulation reproduced a surface ECG similar to the one recorded during spontaneous VT). The fact that the site of origin of the VT is never in the same point of the earliest endocardial activation during sinus rhythm and the fact that this site is located in a zone with rich terminations of the conduction system, suggest the reciprocating VT may develop in a circuit, with both conduction and myocardial tissue.

[The endocardial ventricular activation map in a case of intermittent BBS in phase III (author's transl)]. / Mappa dell'attivazione ventricolare endocardica in un caso di blocco di branca sinistra (BBS) intermittente (BBS in fase 3).

To obtain information on endocardial activation-sequence, unipolar recordings at seven left ventricular and six right ventricular points were performed in a 37-year-old man suffering from cardiomyopathy and tachycardia-dependent left bundle branch block (LBBB). Results were as follows: 1) the recovery time was longer in anterior than in posterior portion of left bundle branch fibers; 2) an high posterior left ventricular point was directly activated via posterior left bundle branch fibers; 3) the directly activated left ventricular zone was too small and relatively too late excited in respect of the right interventricular septum, from which the stimulus reached the left septum, to mask the LBBB electrocardiographic pattern; 4) in the presence of tachycardia-dependent LBBB the duration of left ventricular endocardial activation was about twice (62 msec) that found in the absence of tachycardia-dependent LBBB (28 msec).