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In order to re-evaluate the significance and diagnostic value of electrocardiographs (ECG) and vectocardiographic (VCG) criteria for left ventricular hypertrophy (LVH), 56 hypertensive patients were studied by M-mode echocardiography, ECG and VCG. Parietal thickness (S $ PW) was normal (< 22 mm) in 34 and increased in 22 others. L V diameter was normal in 44, and was increased in 12. The index of left ventricular mass (Devereux-Reicheck) was less than 120 g/m2 in 34 hypertensives and greater than 120 g/sol;m2 in the 22 others.(1) While voltage indices were correlated with LV wall thickness, correlations with mass were less significant. ECG indices were more significant than those for the VCG; the best correlations were obtained for the precordial indices (Sokolow, Lepeschkin, Simonsori), while the remaining indices, including axis, duration, repolarization and surface area, yielded only mediocre correlations.(2) The diagnostic score (sensitivity $ specificity/2) was good for the following ECG voltage parameters: Lepeschkin > 30 (73%); SVI $ R V5–V6 > 30 (72%), Estes score ≥ 4 (72%), and the following VCG criteria: surface > 2 (71%), V max-T angle > 60° (71%). Sensitivity of the voltage indices decreases with dilation of the left ventricular cavity.(3) Grouping of the ECG criteria (duration, repolarization, axis and voltage) resulted in only a minimal increase in the diagnostic score. On the other hand, for the VCG, grouping together the maximum spatial vector, the surface, the QRS-T angle, the initial vector and the duration for analysis, increased the score to 81%.(4) In hypertension, the P wave is an indirect index for LVH. Its duration and the Morris index were better correlated with left ventricular thickness and mass than with the dimensions of the left atrium.(5) Despite sophisticated ECG and VCG analysis the echocardiogram remains the method of choice for the evaluation of LVH. [ABSTRACT FROM PUBLISHER]

Spasm of the left anterior descending coronary artery occurred during cardiac calheterization in a 52 year old patient with a history of syncope and a chest pain syndrome. The main feature of coronary spasm was left axis deviation consistent with left anterior fascicular block. Electrical axis reverted to normality after sublingual nitroglycerin. Coronary angiography was repeated and showed a normal coronary artery tree. This report documents axis shift as a feature of coronary spasm and supports the concept ofischemic left anterior hemiblock. [ABSTRACT FROM PUBLISHER]

Three patients with partial atrial electrical standstill are described. Serial electrocardiograms and electrophysiological studies were performed after a clinical follow-up ranging from four to ten years. Two patients had valvular heart disease and one patient had a sick sinus syndrome. Case I presented, on the admission electrocardiogram, an atrioventricular (AV) junctional rhythm whereas paroxysmal atrial fibrillation had been previously documented. Case 2, who had had long-standing atrial fibrillation presented on admission absence of fibrillation waves and simulated AV junctional rhythm. In case 3 with known sino-atrial block, electrocardiographic monitoring showed sinus rhythm with episodes of slow AV junctional rhythm. Atrial endocardial mapping showed an electrically silent area ranging from a small region near the sinus node (case 1) to the entire right atrium except for a discrete area near the tricuspid valve (case 2). AV dissociation between the electrical activity recorded in the remaining atrium and the junctional escape rhythm was present in every patient. The clinical and electrophysiological features of this entity are reviewed. This study emphasizes the limitations of the electrocardiogram in making the diagnosis of atrial standstill. However, partial atrial electrical standstill should be suspected in patients with AV junctional rhythm or atrial fibrillation with fine waves. This diagnosis may have important therapeutic implications. [ABSTRACT FROM PUBLISHER]

The purpose of the present study was to investigate the effects of low concentrations of nifedipine on the cat myocardium under normal conditions, and during hypoxia with subsequent reoxygenation, and, thus, to find out whether the protective effect on hypoxic myocardium described by different investigators existed at these levels. Experiments carried out on five series of each 10 papillary muscles showed that:(1) Nifedipine (0.02 μg/ml) exerted a negative ino tropic effect on maximum unloaded velocity of shortening and total force (Vmax: 92.91 ± 2.92%; PF: 92.10 ± 2.60%), whereas depression of peak velocity of relaxation became marked only at 0.2 μg/ml (Vrelax: 88.87 ± 3.91%). This dose-dependent effect is also Ca$ $-dependent.(2) Nifedipine (0.02 μ/ml) protected against the depression of Vmax, PF and Vrelax during hypoxia (PO2 = 25 mm Hg) Vmax: 82.60 ± 3.45% v. 78.45 ± 1.35% control; PF: 54.65 ± 4.41% v. 48.74 ±3.51% and Vrelax: 92.55 ± 4.50% v. 68.47 ± 1.30%).(3) The association of nifedipine (0.02 μ/ml) and nitroglycerin (0.3 μ/ml) accelerated the recovery of the depression of peak velocity of relaxation during reoxygenation (Vrelax: 99.90 ± 5.63% v. 89.96 ± 5.15% nifedipine alone). [ABSTRACT FROM PUBLISHER]

Patients with a particular thrombotic profile may be at greater risk of myocardial infarction during coronary artery bypass graft surgery. The thrombotic profile of 50 patients admitted to hospital with stable angina pectoris was determined prior to haemodynamic investigation. ECG results and determination of cardiac enzymes showed that 12 patients had suffered a perioperative myocardial infarction. These patients had a higher mean atherosclerotic score (42.1 ± 10.5 vs 32.9 ± 13, P<0.02), a longer aortic cross clamp time (59 ± 15.2 vs 45.7 ± 16.3 min, P < 0.05), lower serum levels of protein C (101.2±26 vs 124.7+ 31.4%, P<0.05) and tissue plasminogen activator (322 ± 580 vs 2307±2830 IU ml, P<0.01). There were no differences between the two groups in Jenkin's coronary score, the number and type of grafts, ejection fraction, left ventricular end-diastolic pressure, lipid profile or levels of markers of platelet release. In addition to a more severe distal coronary atheroma and a longer aortic cross-clamp time, patients with impaired endothelial fibrinolytic activity appeared to be at greater risk of myocardial infarction during coronary artery bypass graft surgery. [ABSTRACT FROM PUBLISHER]

Spontaneous coronary artery dissection is a rare disease with a higher prevalence in women, especially in the post-partum state. In one case, we attempted to relate this pathology to a disorder in collagen metabolism. A 32-year-old woman presented two episodes ofmyocardial infarction, 2 and 4 months after delivery which were shown to be due to two consecutive coronary artery dissections on coronary angiogram. Collagen metabolism was investigated in skin fibroblast cultures derived from the patient, and in control fibroblast cultures. After protein labelling in culture, total protein and collagen synthesis were determined. Quantification of procollagen synthesized in cell cultures and their rate of conversion into collagen were determined both in the culture media and a cell layer extract by DEAE cellulose chromatography. The results showed a reduced total collagen synthesis in the cultures of the patient in comparison with control cultures. The ratio between type I and III procollagen was not altered. The rate of conversion of procollagen into collagen was higher in the pathological cultures than in control cultures. Impaired collagen synthesis due perhaps to a change in hormonal equilibrium in the post-partum state might therefore have been responsible for coronary artery dissection. [ABSTRACT FROM PUBLISHER]