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Biomedical subjects

D Mathey

Publications and source records attributed to D Mathey.

At least 55 records · Page 3Linked to original sources
PubMed1979

[Anti-arrhythmic effect of tocainide (lidocaine congener) on ventricular arrhythmias (author's transl)].

The antiarrhythmic effect of tocainide, an amine analogue of lidocaine, was tested in the course of a double-blind trial on 12 patients with ventricular arrhythmias. Daily dose was 400 or 600 mg every eight hours. In all tested patients the frequency of ventricular extrasystoles, analysed by means of ambulatory 24-hour ECG monitoring, decreased by an average of 70%. In four of nine patients the severity of the ventricular extrasystoles (Lown's classification) was improved by at least one functional class. There was no correlation between the anti-arrhythmic effect and the plasma level of tocainide, which was between 4.1 and 9.7 micrograms/ml. Four patients had side effects in the form of CNS symptoms, but the drug did not have to be discontinued. Tocainide is an orally effective antiarrhythmic drug, an alternative in the treatment of ventricular arrhythmias.

Adult↗
PubMed1979

Assessment of left ventricular filling by echocardiography in normal subjects and in subjects with coronary artery disease and with asymmetric septal hypertrophy.

To examine the time course of left ventricular filling, a computerized analysis of echocardiograms was performed in 16 normal subjects, 10 patients with coronary artery disease (CAD) but no cardiac enlargement and 7 patients with asymmetric septal hypertrophy (ASH). After hand-controlled digitization of the echocardiogram, a plot of the left ventricular diameter time-curve demonstrated separate phases of rapid filling, slow filling and atrial contribution. The left ventricular diameter at end-systole and at the end of the three diastolic phases was determined by pattern analysis of the diameter-time curve. On analysis of successive beats in the normals, the coefficient of variation for each of these four values of the left ventricular diameter was less than +/- 5%. Between CAD, ASH and normals there was no significant difference in left ventricular end-diastolic diameter, nor in the extent and percentage of diameter shortening during systole. In contrast, abnormalities of the filling pattern were found in CAD and ASH. The maximal rate of diameter lengthening was not different in CAD (13.0 vs 13.7 cm/sec in normals, N.S.) but decreased in ASH (9.3 cm/sec, p less than .01). The percentage of diameter lengthening occurring in the rapid filling phase was decreased in both patient groups (55% in CAD and ASH vs 73% in normals, p less than .001). The slow filling phase did not contribute to more diameter lengthening (13% in CAD and 17% in ASH vs 12% in normals, N.S.). In CAD and ASH, the atrial contribution was markedly increased (33% in CAD and 28% in ASH, vs 15% in normals, p less than .001), and there was a higher rate of diameter lengthening during the atrial contraction (7.6 cm/sec in CAD, p less than .001 and 5.7 cm/sec in ASH, p less than .01, vs 3.1 cm/sec in normals). In conclusion, after computer processing, noninvasive measurements of the left ventricular diameter allows to identify a typical filling pattern in patients with CAD and ASH, consistent with an abnormal compliance of the left ventricle and a compensatory increased atrial contribution.

Adult↗
PubMed1979

[Left ventricular relaxation and filling abnormalities in patients with HOCM and left ventricular pressure overload (author's transl)].

In order to test the hypothesis that delayed mitral valve opening (MO) with regard to endsystolic dimension (t DS-MO) is specific for hypertrophic obstructive cardiomyopathy (HOCM), LV echograms of patients with different forms of LV hypertrophy due to chronic pressure overload (CPO; aortic stenosis + arterial hypertension, n = 24) and hypertrophic obstructive cardiomyopathy (n = 24) were recorded, digitized and compared with those of normals (N :n = 28(. In patients with HOCM (93 +/- 37 ms; p less than 0.0001) and CPO (66 +/- 31 ms; p less than 0.0001) the time t DS-MO was significantly delayed compared with N (13 +/- 15 MS), due to abnormal relaxation. This prolonged relaxation time resulted in an abnormal diameter increase (delta D) during the isovolumic relaxation phase (HOCM: 4.0 +/- 2.2 MM/CPO: 3.0 +/- 1.8 mm; p less than 0.0001/N:0.6 +/- 0.5 mm) and the rapid filling phase (HOCM 7.6 +/- 2.7 mm; p less than 0.0001/CPO 9.2 +/- 2.9 mm; p less than 0.05 / N: 10.7 +/- 2.2 mm). The echocardiographical signs of an abnormal relaxation are not specific for HOCM, they can be seen in different forms of secondary LV hypertrophy and are accompanied by changes in the diastolic filling pattern.

Adolescent↗
PubMed1978

[Reversible myocardial ischaemia or irreversible myocardial fibrosis? Differentiation by biphasic 201thallium scintigraphy (author's transl)].

The results of biphasic 201thallium (201Tl) scanning were compared with those of coronary arteriography, left ventricular angiogarphy and stress ECG in 56 patients with coronary artery disease and six with no evidence of heart disease. There were 104 201Tl defects, 50 of them reversible. The defects were always located in the area supplied by a critically stenotic coronary artery. Correlation of regional wall motion with 201Tl activity demonstrated that in all forms of abnormal wall motion there was either ischaemia or fibrosis. The resting LV angiogram thus does not make it possible to distinguish between myocardial ischaemia and fibrosis. Taking the LV angiogram as a standard, the rate of false-positive 201Tl scintigrams was 5%, that of false-negative ones 23%. The biphasic 201Tl scintigram was more sensitive than the stress ECG in detecting myocardial ischaemia. It furthermore made it possible to localize the ischaemic (or fibrotic) region within the LV and to estimate its size.

Adult↗
PubMed1978

[Short-term localized myocardial ischaemia and its consequences in Prinzmetal angina pectoris (author's transl)].

In a 45-year-old female patient with Prinzmetal angina pectoris coronary angiograms and a 201thallium scintigram were performed during an ergotamine-induced episode of angina. The spontaneous and the ergotamine-induced attacks were characterized by transient ST elevation in the posterior wall ECG leads. The coronary angiogram during the attack showed spasm of the circumflex branch of the left coronary artery. In the 201thallium scintigram a large defect in myocardial thallium uptake was noticed in the posterior wall of the left ventricle. Angina and ECG abnormalities disappeared within 4 minutes. However, the scintigraphic defect disappeared only after 6 hours. The slow recovery of myocardial thallium uptake is thought to represent an alteration of the myocardium after a brief 4 minute interruption of regional coronary arterial blood flow. The diagnostic approach in patients with Prinzmetal angina is discussed.

Angina Pectoris↗
PubMed1978

LV filling in IHSS.

Explore the source record for details and available documents.

Cardiomyopathy, Hypertrophic↗
PubMed1977

Left ventricular hemodynamics and function in acute myocardial infarction: studies during the acute phase, convalescence and late recovery.

The left ventricular hemodynamics of 70 patients with acute myocardial infarction were determined from measurements of pulmonary arterial end-diastolic pressure, cardiac index, mean arterial pressure and heart rate during the acute phase(first study, 5 hours after admission), 4 to 6 weeks later (second study, during convalescence) and in 35 percent of all subjects 6 to 12 months after the acute infarction (third study). Serial analysis of serum creatine kinase was carried out during the acute phase. The peak CK value normalized for body surface area was used as a rough index of the extent of the acute myocardial necrosis. The condition of all survivors of the acute stage improved. Patients with only slightly reduced left ventricular performance during the acute stage recovered to nearly normal during convalescence. The condition of patients with greatly reduced left ventricular function also improved but remained impaired during convalescence. In all patients the main changes in left ventricular hemodynamics occurred within the first 4 to 6 weeks; there was almost no further alteration during the following 9 months.

Acute Disease↗
PubMed1977

Infarct size estimated from serial serum creatine phosphokinase in relation to left ventricular hemodynamics.

In 50 patients with proven acute myocardial infarction (AMI), left ventricular hemodynamics (pulmonary end-diastolic pressure [PAEDP]; cardiac index [CI]; stroke volume index [SVI]; and SVI/PAEDP were related to the size of the acute infarct. Acute infarct mass was calculated from serial determinations of serum creatine phosphokinase (CPK) every two hours, using a computer program. In 15 cases postmortem measurement of acute infarct size after staining with Nitro-BT was made and correlated with calculated infarct size. Correlation in this limited number of cases was good with a mean difference of 7 g. Acute infarct mass in 38 survivors was 46 +/- 5 g and was significantly smaller (P less than 0.05) than in the 12 nonsurvivors (76 +/- 12 g.) PAEDP in surviving patients was significantly lower (17 +/- 1 mm Hg) and SVI (36 ml/m2) and SVI/PAEDP (2.4 ml/m2/mm Hg) significantly higher than in the nonsurvivors (PAEDP: 24 mm Hg; SVI: 23 ml/m2; SVI/PAEDP: 0.86 ml/m2/mm Hg) (P less than 0.001 for all differences). Similar significant differences were observed between patients not in shock and those in cardiogenic shock. Although in 39 patients, in whom the infarction was their first, infarct mass was larger (58 +/- 6 g) than in 11 patients with repeat infarctions (37 +/- 8 g), left ventricular hemodynamics were slightly more impaired in reinfarctions (PAEDP: 21 +/- 3 mm Hg; CI:2.60 L/min/m2) than in first infarctions (PAEDP: 18 +/- 1 mm Hg; CI:2.82 L/min/m2). The occurrence of cardiogenic shock was a strong predictor of death; however, the wide scatter of the data for the parameters cardiac index, PAEDP, and acute acute infarct mass precluded their usefulness, when taken individually, in predicting survival. When a relationship between hemodynamics and infarct size was looked for, four constellations of individual patients were identified. These groups were defined by PAEDPs of above or below 18 mm Hg and infarct sizes above or below 65 g. Class A patients (N = 22) had a small infarct (29 +/- 4 g) and good pump function (PAEDP: 13 mm Hg; SVI: 40 ml/m2; SVI/PAEDP: 3.27 ml/m2/mm Hg); prognosis was good for these patients. In class B (N = 13) the infarct was large (96 +/- 8 g) and pump function markedly impaired (PAEDP: 26 mm Hg; SVI: 24 ml/m2; SVI/PAEDP: 0.98 ml/m2/mm Hg); 54% of these patients died. Five patients in class C had, in the presence of a large infarct (84 g), only a slightly elevated PAEDP of 17 mm Hg and an almost normal SVI of 37 ml/m2. In contrast, the ten class D patients had an infarct size (34 g) similar to that in class A, but high PAEDP (23 mm Hg) and moderately reduced SVI (31 ml/m2). In this group a high incidence of reinfarctions (six out of ten) occurred. It is concluded that infarct mass calculated from serial CPK analysis, as a single parameter, cannot be used to predict mortality or development of cardiogenic shock in an individual patient.

Acute Disease↗
PubMed1976

[Significance of the size of an acute infarct for left ventricular haemodynamics (author's transl)].

Acute infarct size was estimated from serial determinations of creatine-kinase (CK) activity. In 15 patients the infarct size was obtained post-mortem, using nitro-blue-tetrazolium stain. There was good correlation between the two measurements (r = 0.98). The relationship between the calculated infarct size and haemodynamic values was obtained in 50 patients (end-diastolic pulmonary arterial pressure [PAEDP], cardiac output, stroke volume, stroke volume/filling pressure of left ventricle [SVI/PAEDP]). On average there was a tendency towards impaired left ventricular haemodynamics with increasing infarct size. Among the survivors the infarct size (51 g) was significantly less (P less than 0.05) than that of those who had died (83 g). PAEDP at 24 mm Hg was significantly higher in those who died than in the survivors (17 mm Hg), cardiac index was 2.95 l/min-m2 in the survivors compared with 2.14 l/min-m2, while SVI/PAEDP was 2.4 ml/m2-mm Hg in the former and 0.9 ml/m2-mm Hg in the latter. However, in individual cases the infarct size sometimes did not correlate with haemodynamic values. Taking into account infarct size and haemodynamics, four classes could be distinguished: (a) infarct size less than 65 g with good haemodynamics (PAEDP less than 18 mm Hg, normal cardiac index); (b) infarct size greater than 65 g with PAEDP greater than 18 mm Hg and markedly reduced cardiac index). Only 10% of those a to c had previously had infarcts, compared with 60% of those in class d (infarct less than 65 g, PAEDP above 18 mm Hg). Small infarcts with markedly impaired haemodynamics thus indicate that there has been previous damage to remaining myocardium.

Acute Disease↗
PubMed1976

[Intra-atrial conduction disorders of 2d degree].

Five patients with second degree intraatrial block are presented. The first three cases had a sick sinus syndrome with sinus bradycardia, broad P waves and episodes of atrial flutter or fibrillation. In these patients a Wenckebach phenomenon could bei elicited by atrial stimulation at a critical driving rate between the stimulated site and the recording electrode. In the first patient this conduction disturbance was obtained at several right atrial stimulation sites. The block could be elicited in the other two patients only in a limited area of the right atrium respectively only by left atrial pacing. In the remaining two patients an atrial tachycardia with block was observed. The intraatrial conduction disturbance was manifested as an exit block around the ectopic pacemaker. In one patient the tachycardia was induced by digitalis intoxication. In the other patient no etiologic factor of the tachycardia could be found. While the first three patients presented intraatrial conduction disturbances already in sinus rhythm, the last two cases showed after recovery from the atrial tachycardia P waves of normal duration and configuration.

Aged↗
PubMed1975

Creatine kinase release in acute myocardial infarction: correlation with clinical, electrocardiographic, and pathological findings.

Creatine kinase (CK) release curves were analysed in 40 patients with acute myocardial infarction. Three groups could be identified. Group A (duration of CK release less than 30 hours) comprised 15 patients whose CK release was completed within 22.8 hours. In these patients chest pain was noted on the first hospital day and necropsy in three showed a homogeneous myocardial infarction. Group B (duration of CK release greater then 30 hours) comprised 16 patients who had a significantly longer CK release time of 42.2 hours (P less than or equal to 0.05). Their chest pain persisted for two to three days and pathological examination in five patients showed a heterogeneous composition of the infarcted myocardium. Group C comprised nine patients who had a second rise of serum CK. This was always associated with chest pain. It reflected an extension of the infarct which accounted on average for 24 per cent of the size of the final infarct. We concluded that a CK release of short duration indicated infarction without extension, CK release of longer duration indicated a gradual extension of infarction, and a repeated CK release resulted from a sudden extension of an infarct. According to these criteria an extension of the infarct occurred in 62 per cent of our patients.

Aged↗