Biomedical subjects

P Assayag

Publications and source records attributed to P Assayag.

59 records · Page 4Linked to original sources

PubMed1984

Aortic input impedance in heart failure: comparison with normal subjects and its changes during vasodilator therapy.

This study was aimed at the evaluation of aortic impedance in patients with congestive heart failure. Aortic impedance (simultaneous measurements of aortic pressure and blood flow), mean (Wm) and pulsatile (Wp) powers were compared in 11 normal subjects and in 12 patients with heart failure. Pulse wave velocity (C: modified Moëns-Korteweg equation, simultaneous measurements of aortic pressure and radius) was determined under control conditions in all normal subjects and in 7 patients with heart failure. Impedance curves in patients with heart failure were characterized by increased values of the impedance modulus at 0 Hz (peripheral resistance) and at low frequencies. The characteristic impedance, C, and phase were not different from normal subjects. In six patients with heart failure, impedance curves were studied during nitroprusside infusion. During the infusion of the vasodilator, the impedance modulus at 0 Hz and at low frequencies decreased. The characteristic impedance was unchanged. The zero intercept of the phase was shifted towards lower frequencies. These results show that the changes in impedance curves in patients with heart failure are due to greater peripheral resistance and wave reflection. During nitroprusside infusion the stroke volume increased and the aortic blood flow became more pulsatile (greater values of low frequency components). This modification accounts for the increased values of Wm and Wp, and is related to decreased peripheral resistance and wave reflection.

Adult↗

PubMed1984

[Anti-arrhythmic effect of oral propafenone. Apropos of 70 cases].

During a 3 year period, seventy patients aged 53 +/- 16 years with a total of 73 arrhythmias were treated over a mean period of 6.8 months (maximum 27 months) with oral propafenone, the usual dose being 900 mg/day. The study covered the whole spectrum of cardiac arrhythmias (32 supraventricular, 41 ventricular), and their relation to the autonomic nervous system. The efficacy was scored from 1 (no effect) to 5 (complete control) as judged by the clinical response, the results of Holter monitoring (175 control and 133 test recordings on therapy), and a comparison was made between the effects of propafenone and other antiarrhythmics: quinidine-like drugs, beta-blockers and amiodarone. With respect to supraventricular arrhythmias: 9 cases of vagally-induced atrial flutter and fibrillation were unaffected by propafenone (mean score = 1.1). On the other hand, the drug was very effective (mean score = 4.1) in 8 cases of adrenergic atrial arrhythmias. In 12 arrhythmias with more varied mechanisms (extrasystoles, tachysystole, paroxysmal atrial fibrillation) an intermediate score was obtained (2.8). Three cases of resistant junctional tachycardia due to reentry were improved. At ventricular level, 5 cases of extrasystole sensitive to quinidine were also improved by propafenone (4.6); the difference was more clearcut in 8 cases of benign idiopathic tachycardia (propafenone: 4.1, and quinidine: 2.4). This was more marked in 13 cases of more severe arrhythmia in diseased hearts in which the effect of propafenone (4.1) was superior even to that of amiodarone. However, propafenone was less effective (3.3) than amiodarone in 4 cases of severe polymorphic idiopathic ventricular tachycardia closely related to the autonomic nervous system. The antiarrhythmic effect of propafenone was appreciable in 10 cases of resistant post-infarction ventricular tachycardia, eventually in association with amiodarone. Slowing of the sinus rhythm (-11.6%) with no change in the day/night ratio was due to beta-inhibition. However, in toxic doses this may progress to sinoatrial block (9 cases). A lengthening of the PR interval and duration of QRS was common, but this was not complicated by torsade de pointes, one case of which was successfully treated by propafenone. Secondary gastro-intestinal effects and vertigo were rarely severe enough to warrant stopping therapy. In conclusion, these results show that the introduction of propafenone is a valuable therapeutic advance in the treatment of arrhythmias, especially in those with a favoring adrenergic mechanism.

Administration, Oral↗

PubMedDate not supplied

Residual area at risk after anterior myocardial infarction: are ST segment changes during coronary angioplasty a reliable indicator? A comparison with technetium 99m-labeled sestamibi single-photon emission computed tomography.

BACKGROUND: The aim of this study was to assess whether, after anterior myocardial infarction, ST segment changes during percutaneous transluminal coronary angioplasty (PTCA) of the left anterior descending coronary artery correlated with the amount of ischemic myocardium in the area at risk, measured with 99mTc-labeled sestamibi single-photon emission computed tomography (SPECT) during balloon inflation. METHODS AND RESULTS: Quantitative continuous monitoring of the ST segment was performed during PTCA of the left anterior descending coronary artery in 11 patients, and corresponding SPECT imaging was compared with a rest acquisition performed before PTCA. SPECT was quantified by a bull's-eye analysis according to main criteria: (1) the planimetered defect size during PTCA as an indicator of the size of the area at risk, (2) the change in the pathologic/normal area count ratio in the area at risk as an index of the severity of ischemia, and (3) the difference between the size of the defect during PTCA and at baseline. ST segment changes were correlated to the variation in pathologic/normal area count ratio (19% +/- 14%; r = 0.61; p < 0.05) but not to the sizes of the scintigraphic defects. CONCLUSION: ST segment changes induced by occlusion of the infarct-related coronary artery during PTCA are related mostly to the severity of ischemia rather than to the size of the area at risk.

Adult↗

PubMedDate not supplied

MRI and cine MRI of asymmetric septal hypertrophic cardiomyopathy.

OBJECTIVE: This study was designed to determine MR and cine MR characteristics of asymmetric septal hypertrophic cardiomyopathy and to correlate MR and cine MR features with the severity of left ventricular outflow tract obstruction. MATERIALS AND METHODS: Ten consecutive patients with asymmetric septal hypertrophic cardiomyopathy [resting obstructive (n = 3), latent obstructive (n = 4), nonobstructive hypertrophic (n = 3)] and five healthy volunteers underwent MRI and cine MRI. Oblique two chamber and four chamber views were obtained in all cases. RESULTS: In the 10 patients, the mean +/- SD end-diastolic myocardial thickness was 22.7 +/- 6.3 mm in the basal septum and 13 +/- 3.9 mm in the posterolateral wall with a ratio of 1.76 +/- 0.30; the corresponding values were 10.6 +/- 1.1, 10.4 +/- 1.1, and 1.02 +/- 0.08 mm, respectively, in five healthy volunteers. The mean systolic thickening of the basal septum was 22 +/- 12%. This value was 49 +/- 4% in the five healthy volunteers. In resting obstructive hypertrophic cardiomyopathy, septal wall thickness was > or = 25 mm with a systolic thickening of 10%. A systolic anterior motion of the mitral valve was demonstrated in four patients with resting subaortic pressure gradients ranging from 28 to 120 mm Hg. A signal void area was demonstrated within the left ventricular outflow tract during systole in the seven patients with obstructive cardiomyopathy. This signal void area reached its maximum during early systole in the most severe obstructions and during midsystole in the less severe obstructions. CONCLUSION: In patients with asymmetric septal hypertrophic cardiomyopathy, gross correlation was demonstrated between severity of obstruction and several MR and cine MR features including increased end-diastolic thickness of the septal wall, decreased systolic thickening of the septal wall, systolic anterior motion of the mitral valve, and signal void area within the left ventricular outflow tract during systole.

Adult↗

PubMedDate not supplied

Cine MRI of mitral regurgitation in planes angled along the intrinsic cardiac axes.

OBJECTIVE: This prospective study was designed to evaluate the mechanism and severity of mitral regurgitation (MRG) by means of cine MRI using planes angled along the intrinsic cardiac axes. MATERIALS AND METHODS: In 25 patients with MRG, analysis of the direction, extent, and distribution of left atrial signal void area was performed on both two chamber and four chamber cine MRI views. Cine MRI features including qualitative grading, maximal length of regurgitant jet, and ratio of regurgitant jet area to left atrial area were compared with the results of color flow Doppler (CFD) mapping (n = 25), angiography (n = 20), and regurgitant fraction as determined at catheterization (n = 15). RESULTS: In the four chamber view, cine MRI demonstrated central extension of regurgitant jet (n = 8) in cases with dilatation of valve annulus or retraction of both mitral valve leaflets, anterior extension (n = 8) in cases with prolapse of the posterior leaflet, and posterior extension (n = 7) in cases with prolapse of the anterior leaflet or retraction of the posterior leaflet. In two cases of mild MRG with small signal void area, evaluation of mechanism was not feasible. The results of cine MRI and angiographic qualitative gradings were the same in 19 of the 20 patients and differed by one grade in the other patient. In the 25 patients, maximal length of the regurgitant jet was well correlated with both regurgitant jet area and ratio of the jet area to the left atrial area as determined by CFD mapping (r = 0.91, r = 0.85, p < 0.0001, respectively). In 15 patients the maximal length of regurgitant jet was correctly correlated with regurgitant fraction determined at catheterization (r = 0.76, p < 0.001). CONCLUSION: Cine MRI by means of planes angled along the intrinsic cardiac axes allows assessment of both the mechanism and the severity of MRG.

Adult↗