摘要:

The pathogenesis of angina pectoris in patients with left ventricular hypertrophy secondary to arterial hypertension and with normal coronary arteries remains uncertain. We measured coronary blood flow (argon method) in 12 control subjects and in 16 patients with arterial hypertension at rest and after intravenous administration of dipyridamole (0.5 mg/kg). In the patients with arterial hypertension, coronary blood flow response to dipyridamole was markedly reduced (p < .001 as compared with control values). During coronary vasodilation there was a linear correlation between coronary resistance and left ventricular end-diastolic pressure (r = .67, p < .001). Left ventricular catheter biopsy specimens did not reveal alterations in myocardial microvasculature. These findings suggest that reduction of coronary reserve may be an important contributor to the pathogenesis of angina pectoris in these patients.

ISSN:0009-7322    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

In 14 consecutive patients with variant angina we investigated the possible role of coronary a-adrenergic receptors in the genesis of coronary spasm. In eight patients, computerized, beat-by-beat analysis of the electrocardiogram recorded during continuous Holter monitoring failed to reveal any increase of heart rate and corrected QT interval (both indexes of cardiac sympathetic activation) in the period preceding the onset of ST segment changes in 197 episodes of ischemia caused by coronary spasm. In the same patients, analysis of the circadian distribution of ischemic episodes revealed a significantly higher incidence in the early morning hours, when sympathetic activity is at the lowest level. Twelve patients underwent serial provocative testing with cold pressor, phenylephrine, or norepinephrine infusion and administration of ergonovine maleate. Ergonovine consistently reproduced coronary spasm in all 12 patients, while results of cold pressor testing were positive in only one. Infusion of phenylephrine (eight patients) or norepinephrine after, β-blockade (four patients) failed to precipitate myocardial ischemia. In five patients infusion of phentolamine at the highest tolerated dose did not reduce significantly the number of ischemic attacks when compared with placebo. In contrast to results of previous reports, our data seem to rule out the hypothesis that an increase of sympathetic outflow to the heart plays an important role in the genesis of coronary spasm. We cannot, however, exclude the possibility of localized a-stimulation of epicardial arteries.

ISSN:0009-7322    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

ABSTRACT Platelets have been implicated in the pathogenesis of coronary artery disease, and a number of studies have examined platelet function and coagulation parameters in such patients. We have examined platelet coagulant activities, volumes, and aggregate ratios in 23 patients with chest pain, seven of whom had normal coronary angiograms (group I) and 16 of whom had angiographically proven coronary artery disease (group II). There were no significant differences in the mean values for platelet volume or platelet aggregate ratios between the two groups. The platelet coagulant activities concerned with initiation and the early stages of intrinsic coagulation were significantly increased in patients in group II as compared with those in group I. No significant differences were noted between the two groups with respect to prothrombin time, partial thromboplastin time, and plasma levels of fibrinogen and coagulation factors V and VIII. However, the mean activity in plasma of antithrombin III (but not the level of antithrombin III antigen) was significantly lower in patients of group II compared with group I. Overall, our observations provide evidence for an enhanced contribution of platelets to the intrinsic coagulation system in patients with coronary artery disease. The platelet coagulant hyperactivity noted in these patients may reflect a role of platelets in the pathogenesis of coronary artery disease or may be secondary to the underlying arterial disease.

ISSN:0009-7322    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

ABSTRACT We examined the relationship between changes in heart rate and the measured QT interval of the electrocardiogram in healthy subjects after exercise and during breath holding, hyperventilation, the dive reflex, the Valsalva maneuver, and the cold-pressor test. The tachycardia of exercise was accompanied by the familiar shortening of the QT interval, but substantial heart rate changes encountered in other more “sedentary” maneuvers were accompanied by very small changes in QT. Calculating the corrected QT in the latter instances, therefore, yielded spurious results. The data suggest very little, if any, direct effect of heart rate on the QT interval. The length of the interval in healthy subjects appears to be determined largely by reflexly elicited discrete autonomic influences. Those associated with exercise result in QT shortening but, during neurally mediated cardiovascular adjustments that do not involve exercise, QT is maintained within narrow limits.

ISSN:0009-7322    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

We have recently described the ability of abrupt short-to-long changes in atrial cycle length (CL) to prolong refractoriness of the His-Purkinje system (HPS) and increase the likelihood of aberrant ventricular conduction. We have also shown similar functional behavior in retrograde refractoriness of the HPS during changes in ventricular CL. To further assess these characteristics we evaluated the effect of abrupt short-to-long change in ventricular CL on the phenomenon of macroreentry within the HPS (Re-HPS) in 20 patients in whom Re-HPS occurred during application of a ventricular extrastimulus (V2) at a constant ventricular CL (method 1) and/or with abrupt short-to-long change in CL (method II). For both methods V2was coupled to a CL of identical duration, designated the reference CL (CLR). In method I the CLs preceding (CLp) the CLRequaled CLR, whereas in method II CLP was less than CLR. The results showed a dramatic increase in occurrence of Re-HPS with abrupt short-to-long change in CL with Re-HPS occurring in 19 patients with this method compared with in 11 patients during constant CL. In 10 patients manifesting Re-HPS with both methods the associated retrograde conduction (V2H2) delays were equal or less during abrupt short-to-long changes in CL and, remarkably, there were concomitantly shorter antegrade conduction (H2V3) delays compared with at a constant CL. Moreover, despite the resulting shorter V2V3, additional Re-HPS beats were also more likely to occur with abrupt short-to-long change in CL compared with at a constant CL. These findings suggest that (1) there is an earlier onset or more distal site of retrograde block in the right bundle branch-Purkinje system or Purkinje-myocardial junction with abrupt short-to-long change in CL, which is consistent with previous findings of increased refractoriness of HPS with this method, and (2) that such changes in CL can facilitate reentry involving the HPS.

ISSN:0009-7322    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Studies at necropsy have shown that the cardiomyopathy of Duchenne muscular dystrophy selects the posterobasal and contiguous lateral left ventricular (LV) walls as initial and primary sites of myocardial dystrophy in the absence of small-vessel coronary artery disease in these areas. The present investigation was designed chiefly to determine whether a myocardial metabolic abnormality could be identified in these same areas during a patient's life. Positron emission computed tomography was used to study regional LV metabolism with18F 2-fluorodeoxyglucose, and metabolism and/or perfusion was studied with13NH3. In addition, all subjects had the following performed: thallium-201 scans, technetium-99m multiple-gated equilibrium blood pool imaging, electrocardiograms, vectorcardiograms, and M mode and two-dimensional echocardiograms.18F 2-fluorodeoxyglucose activity was selectively increased in the posterobasal and posterolateral walls of the left ventricle in 11 of 12 patients with technically adequate images, indicating accelerated regional exogenous glucose utilization.13NH3 activity was selectively decreased in the same areas in 13 of 15 patients, indicating either a regional metabolic alteration in uptake and trapping, a reduction in regional blood flow, or both. These data identify a myocardial metabolic abnormality concentrated in specific segments of the LV free wall in living patients with Duchenne dystrophy.

ISSN:0009-7322    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

We performed simultaneous echocardiographic and hemodynamic studies in 11 patients with muscular subaortic stenosis to determine whether systolic anterior motion (SAM) of the anterior mitral leaflet and the pressure gradient are related quantitatively. SAM without septal contact was associated with either no gradient or a small impulse gradient of less than 10 mm Hg. SAM with septal contact was always associated with a pressure gradient of more than 10 mm Hg. The size of the pressure gradient correlated inversely with the time periods: (1) onset of SAM to onset of SAM-septal contact (r = −.79, p < .001) and (2) onset of aortic ejection to onset of SAM-septal contact (r = −.89, p < .001). Size also correlated directly with the time period: (3) duration of SAM-septal contact (r = .80, p < .001). Thus when the time from the onset ofSAM to the onset of SAM-septal contact was long, SAM-septal contact developed late in systole, the duration of SAM-septal contact was brief and the pressure gradient was low. When SAM-septal contact developed in early systole, the duration of SAM-septal contact was long and the pressure gradient was high. With the index of time period (3) divided by time period (1), a regression equation was devised to predict the size of the pressure gradient (pressure gradient [mm Hg] = 25 [ratio] + 25; r = .90, p < .001; SE ± 15mm Hg). The echocardiographic time period index was validated prospectively in nine other patients and the significant correlation with the hemodynamically determined gradient persisted (r = .89, p < .01). We conclude that SAM and the pressure gradient are related quantitatively in muscular subaortic stenosis. These observations have implications regarding the mechanism and significance of the pressure gradient in muscular subaortic stenosis.

ISSN:0009-7322    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

It has been previously suggested that salt loading produces structural changes of the arteries in hypertensive patients who respond to salt loading with a greater rise of blood pressure. This study examined the possibility that salt loading alters venous distensibility in hypertensive patients. Twenty-one patients with essential hypertension were placed on a low-sodium diet (70 meq) for 7 days and then were placed on a high-sodium diet (345 meq) for 7 days. Patients were arbitrarily divided into two groups based on the response of their blood pressure to salt loading: (1) those whose mean blood pressure increased by more than 10% while on the high-salt diet as compared with those on the low-salt diet (salt-responsive patients, n = 8) and (2) those whose mean blood pressure did not increase by more than 10% (salt-nonresponsive patients, n = 13). The venous pressure-volume relationship was determined in the forearm with a water-filled plethysmograph when patients were on the low- and high-salt diet. Venous pressure-volume curves were not different between salt-responsive and salt-nonresponsive patients while on the low-salt diet. High-salt intake shifted the curve toward the pressure axis for salt-responsive patients (p < .05) but not for salt-nonresponsive patients. Phentolamine, 1 mg administered intravenously for 5 min, did not significantly alter venous pressure-volume curves for either group while on the low- or high-salt diet. These results suggest that salt loading decreased venous distensibility in salt-responsive patients, which resulted from nonadrenergic mechanisms: structural changes of the veins could perhaps be included as one of these mechanisms.

ISSN:0009-7322    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Central and regional (hepatic, renal, and limb) hemodynamic data are presented for a normal population (n = 16) and for a group of patients with congestive heart failure (n = 64). The patient population represented a wide spectrum of severity of congestive heart failure. Various relationships between central and regional hemodynamics were analyzed. The results indicate that in congestive heart failure blood flow to hepatic, renal, and limb regions is significantly decreased, and that this decrease is proportional and linearly related to the reduction in cardiac output. The vascular resistances of these regions correlated directly with systemic vascular resistance. Changes in renal vascular resistance and renal blood flow became attenuated as the severity of the heart failure advanced from moderate to severe and at higher levels of systemic vascular resistance. There was little to no correlation between systemic blood pressure and liver, kidney, and limb blood flow for the range of systemic pressures studied.

ISSN:0009-7322    

出版商:OVID    

年代:1984

数据来源: OVID