Activation of blood coagulation in patients with mitral stenosis and sinus rhythm

The aim of this study was to assess whether there is blood coagulation activation in patients with mitral stenosis (MS) and sinus rhythm (SR) and to investigate the value of left atrial spontaneous echo contrast (LASEC) as a predictive sign of increased coagulation activity. Using thrombin-antithrombin III complexes and prothrombin fragment 1+2 as in vivo hemostatic markers, we concluded that there is a hypercoagulable state in patients with MS and SR when LASEC is present.     

Electrocardiographic manifestations of dual atrioventricular node conduction during sinus rhythm

In search of critical genes associated with the mechanism of transforming growth factor-alpha (TGF alpha) action in human ovarian cancer, it was found that TGF alpha stimulates c-myc gene expression in human ovarian NIH:OVCAR-3. The role of c-myc in TGF alpha-stimulated growth of NIH:OVCAR-3 cells was examined by the use of the synthetic antisense-myc phosphorothioate oligonucleotide (OPT). Prior exposure of NIH:OVCAR-3 cells to an antisense-myc OPT inhibited TGF alpha-stimulated cell growth and DNA synthesis in a dose-dependent and sequence-specific manner over 4 days. c-Myc protein expression was down-regulated in the antisense-myc treated cells. These results demonstrate both the specific and durable effects of the antisense-myc OPT. Furthermore, the results suggest a role for c-myc in TGF alpha-stimulated cell proliferation.     

Short deceleration time of mitral inflow E velocity: prognostic implication with atrial fibrillation versus sinus rhythm

The present study retrospectively identified 367 patients who had restrictive physiology as defined by deceleration time < or = 130 msec; 293 were in sinus rhythm (SR) (194 men and 99 women; mean age 64 +/- 14 years) and 74 were in atrial fibrillation (AF) (51 men and 23 women; mean age 72 +/- 11 years; p < 0.001). Both groups had similar underlying diagnoses and no significant difference in Doppler indices (E wave, 96 +/- 23 vs 99 +/- 22 cm/sec in SR and AF, respectively; deceleration time, 116 +/- 12 vs 116 +/- 13 msec; and left ventricular outflow tract time velocity integral, 14.8 +/- 4.8 vs 14.5 +/- 4.4 cm). Left ventricular ejection fraction was significantly lower in SR patients (29% +/- 16% vs 39% +/- 20%; p = 0.0003). There were 120 deaths (41%) in the SR group and 35 (47%) in the AF group (median follow-up for both groups, 2.2 years). Restrictive physiology as defined by Doppler echocardiography (deceleration time < or = 130 msec) appears to predict a similar poor prognosis with AF as with SR.     

Mitral annulus size in isolated mitral stenosis

M-mode and two-dimensional echocardiographic images were obtained using the planimeter method in the short axis view and calculated by Doppler-derived pressure half-time in 24 patients with mitral stenosis before and after surgical commissurotomy and posterior annuloplasty. The diameter of the mitral valve annulus was measured in the standard long axis view and in the apical four-chamber view using two-dimensional echocardiography. Preoperatively, the mitral annulus was dilated in all patients as a consequence of left atrial dilation. This could be one of the factors causing residual regurgitation after surgical mitral commissurotomy. However, more data are needed to demonstrate that annuloplasty can prevent the development of mitral regurgitation after surgery.     

Coronary atherosclerosis in subjects with mitral stenosis

The coronary arteries were examined in 60 specimens from patients with mitral stenosis. In three, localized obstruction was nonatherosclerotic in nature (in one, arterial dysplasia; in two, embolic). In 18 of the remaining 57 cases (31.5%), significantly obstructive atherosclerosis in one or more segments of the coronary arterial system was found. This represented 46% of the males and 27% of the females. The incidence of involvement of three or more arteries by significantly obstructive atherosclerosis was 39%, while in a cited series of subjects with angina pectoris three or more vessels were involved in 79% of the cases. It may be concluded that, on the average, the distribution of lesions in patients with mitral stenosis and significant coronary atherosclerosis is less wide than in subjects with clinical coronary disease.     

Pathology of mitral valve stenosis and pure mitral regurgitation--Part I

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant mitral valves. In Part I, conditions producing mitral valve stenosis are reviewed. In over 99% of stenotic mitral valves, the etiology is rheumatic disease. Other rare causes of mitral stenosis include congenital malformed valves, active infective endocarditis, massive annular calcium, and metabolic or enzymatic abnormalities. In Part II, conditions producing pure mitral regurgitation will be discussed. In contrast to the few causes of mitral stenosis, the causes of pure (no element of stenosis) mitral regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendinae.     

Causes of recurrences of mitral stenosis

The authors present an analysis of the late results of closed mitral commissurotomy in 364 patients (maximum terms of observation--17 years). Main causes of recurrent mitral stenosis were recognized: activation of a rheumatic process (50%), nonspecific scarring processes (27%), inadequate commissurotomies (11.1%) and others (11.1%). The routine antirheumatic therapy (bicillin+salicylates) was found to be ineffective in prophylaxis against mitral restenoses. Recurrent mitral stenosis proved to occur more frequently in patients operated upon in young age (under 30).     

Automatic regulation of sinus rhythm in patients with migraine

The clinical symptoms of migraine point to autonomic disturbances, especially to disrupted regulation of the circulatory system and autonomic balance. Searching for more accurate autonomic system studies we turned to the spectral analysis of cardiac rhythm changes, that allows to estimate the autonomic balance in sinus node. 44 patients with migraine were studied and the results were compared with those obtained in 74 healthy subjects. The reduced influence of both sympathetic and parasympathetic part of autonomic system on the sinus rhythm in migraine patients was found. The autonomic balance is shifted to the parasympathetic innervation side in patients with migraine.     

Propranolol serum levels during twenty-four hours

Propranolol serum levels during a 24-hr period were determined every 2 hr in 9 hospitalized patients with angina pectoris after oral administration of 40 mg of propranolol 3 times a day. After the first, second, and third tablets the mean maximum serum propranolol concentrations averaged 118 +/- 71 ng/ml, 134 +/- 97 ng/ml, and 118 +/- 94 ng/ml and the mean minimum concentrations averaged 21 +/- 18 ng/ml, 45 +/- 25 ng/ml, and 54 +/- 34 ng/ml (+/-SD), respectively. These data show a very wide inter- and intraindividual variation in serum propranolol levels. No relationship was found between serum level and blood pressure or dose (related to body weight).     

Retrograde Purkinje potential activation during sinus rhythm following catheter ablation of idiopathic left ventricular tachycardia

We describe two patients with idiopathic left ventricular tachycardia that were cured by radiofrequency catheter ablation. Tachycardia was inducible by ventricular stimulation and was verapamil sensitive. Two distinct presystolic potentials (P1 and P2) were recorded during tachycardia in the mid-septal or inferoapical area, but only one potential (P2) was recorded during sinus rhythm. After catheter ablation at this site, the P1 potential was noted after the QRS complex during sinus rhythm, while the P2 was still observed before the QRS complex. The P1 potential showed a decremental property during atrial or ventricular pacing. These data suggest that Purkinje tissue with decremental properties was responsible for the tachycardia mechanism, and that the reentry circuit involving this tissue is likely to be of considerable size.     

Spectral analysis of short term R-Tapex interval variability during sinus rhythm and fixed atrial rate

Analysis of heart rate variability has been proven useful in stratifying post myocardial patients at risk and in evaluating autonomic dysfunction. Recently augmented inter-lead variability of the QT interval has been associated with increased mortality as a result of arrhythmia and proposed as a marker of dispersion of ventricular repolarization. As the duration of the QT interval is largely dependent upon the length of the preceding cardiac cycle it is tempting to analyse whether neural mechanisms might also directly exert additional modulation. Using autoregressive algorithms we therefore analysed RR and R-Tapex interval variabilities in 15 normal subjects during sinus rhythm and in six patients with a fixed atrial rate. In controls mean R-Tapex interval and variance measured on the vector magnitude were, respectively, 245 +/- 6 ms and 5.1 +/- 0.7 ms2. Spectral analysis of R-Tapex indicated the presence of two spectral components which corresponded to the low and high frequency components of heart rate variability. In R-Tapex variability, high frequency (44 +/- 4 nu) was predominant over low frequency (29 +/- 4 nu). During controlled respiration, a manoeuvre associated with enhanced vagal modulation of sinus node, there was a further increase in high frequency (58 +/- 4 nu) whereas during tilt the low frequency component of R-Tapex variability became predominant (57 +/- 6 nu). In patients with a fixed atrial rate, variance was extremely low (3 +/- 0.9 ms2) and only a respiration-related high frequency component was recognizable in spectral analysis of RR and R-Tapex variabilities. This component was likely to depend upon mechanically induced changes in cardiac vector orientation. These data indicate that during sinus rhythm short-term R-Tapex interval variability is characterized by the same rhythmical components present in RR variability. However, the presence of a very low variance and of only a high frequency component in patients in whom the physiological variability of sinus node is abolished by atrial pacing. suggests that neural modulatory mechanisms do not exert a direct effect on the length of the R-Tapex interval.     

Diagnosis and differential therapy of mitral stenosis

The aim of this study was to investigate the role of metabolic activation in the olfactory toxicity of methyl iodide (MeI). Adult male rats were exposed via nose-only inhalation to 100 ppm MeI for 0-6 h, and non-protein sulphydryl (NP-SH) concentrations determined in selected tissues. Depletion of NP-SH occurred in all tissues, but was most marked and rapid in the respiratory epithelium of the nasal cavity and the kidney. Olfactory, lung and liver NP-SH levels were affected to a lesser extent, and those of the brain declined by only 20-30% over the whole time course. In order to modulate glutathione (GSH) status, animals were pre-treated with (1) phorone plus L-buthionine sulphoximine (BSO), which depleted NP-SH levels in all the tissues examined, or (2) the isopropyl ester of GSH (IP-GSH), which was shown to replenish NP-SH concentrations in all tissues except the liver of animals previously administered phorone. When animals were pre-treated with phorone plus BSO and then exposed to 100 ppm MeI for 2 h, there was a potentiation of the toxicity of MeI as judged by the clinical observations on the animals. In contrast, treatment with IP-GSH prior to and during exposure to MeI for 4 h afforded a marked protection to the olfactory epithelium. In order to inhibit cytochromes P450, animals were pre-treated with cobalt protoporphyrin IX. This decreased hepatic cytochrome P450 concentrations by > 90%, but when animals were then exposed to 100 ppm MeI for 4 h there was no effect on the severity of the olfactory lesion. These results indicate that conjugation of MeI with GSH is a detoxification rather than an activation pathway. Also, there is no major role for cytochrome P450-dependent oxidation in the development of the olfactory lesion.