ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Left ventricular biplane cineangiography, micromanometry, and endomyocardial biopsies were performed in 27 patients with aortic stenosis (AS) and in 17 patients with aortic insufficiency (AI). Twenty-three patients with AS and 15 with AI were restudied at an intermediate time (18 months after successful valve replacement), and nine patients with AS and six with AI were restudied late (70 and 62 months after surgery). Biopsy samples were evaluated for muscle fiber diameter, percent interstitial fibrosis, and volume fraction of myofibrils. In control biopsy samples obtained from five donor hearts at transplantation, these morphometric variables averaged 21.2, μm, 7.0%, and 57.2%, respectively. After surgery, mass determined by cineangiography decreased from 186 to 115 and 94 g/m2in patients with AS and from 201 to 131 and 93 g/m2in patients with AI. At the three studies, muscle fiber diameter was 30.9, 28.0, and 28.7, μm in patients with AS and was 31.4, 27.6, and 26.4 μm in patients with AI. Percent interstitial fibrosis was 18.2, 25.8, and 13.7% in patients with AS and was 20.4, 23.7, and 19.2% in patients with AI. Left ventricular fibrous content decreased from 34.2 to 29.8 and to 12.7 g/m2in patients with AS and from 42.1 to 28.9 and to 18.9 g/m2in patients with AI. Volume fraction of myofibrils was 57.7, 56.8, and 49.0% in patients with AS and was 56.8, 56.6 and 48.8% in patients with AI. Thus, the decrease of muscle mass determined by cineangiography at the intermediate time after valve replacement is mediated by regression of myocardial cellular hypertrophy in patients with AS and AI and in addition by a decrease of fibrous content in patients with AI. Late after surgery, left ventricular fibrous content also decreases in patients with AS. This late decrease associated with minor changes of end-diastolic volume may be important for improvement of increased diastolic myocardial stilfness. Even 6–7 years after valve replacement, incomplete regression of structural abnormalities of left ventricular hypertrophy still exists compared with the normal myocardium. The residually increased relative interstitial fibrosis and the small late postoperative decrease of volume fraction of myofibrils, associated with a prosthesis-related slight left ventricular pressure increase, are at the origin of a persistent systolic overload at the myofibrillar level.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

To describe patterns of an indicator of sudden coronary death, data from the National Center for Health Statistics were examined for deaths occurring out of hospital and in the emergency room (OH/ER) from 1980 to 1985 in 40 states. In 1985, 56% of ischemic heart disease deaths occurred OH/ER among persons aged 35–74 years. The percentage occurring OH/ER declined with age, was higher in men than women, and higher in blacks than whites. At age 55–64, 61% of ischemic heart disease deaths in white and 66% in black men occurred OH/ER. Between 1980 and 1985, age-adjusted death rates in white men aged 35–74 years declined 19%, for OH/ER and 18% for in-hospital ischemic heart disease deaths. The percentage of deaths in ER increased. The decline in deaths occurring OH/ER accounted for 61% of the total absolute decline in ischemic heart disease death rate in white men, 55% in white women, and about 70% in nonwhites. The decline in rates of death OH/ER should encourage further efforts at preventing coronary heart disease and improving emergency medical services.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

To assess the impact of operative reduction of left ventricular outflow obstruction in hypertrophic cardiomyopathy, measurements of great cardiac vein flow, oxygen and lactate content, left ventricular pressures, and cardiac index were measured at rest and during pacing stress in 20 consecutive patients (13, myotomy-myectomy; six, mitral valve replacement; one, both myotomy-myectomy and mitral valve replacement) who underwent both preoperative and postoperative studies. All had angiographically normal epicardial coronary arteries. Operation resulted in reduction in outflow gradient (64±38 to 4±7 mm Hg,p<0.001) and in left ventricular systolic pressuire (186±32 to 128±22 mm Hg, p<0.001) and was associated with reduction in great cardiac vein flow (101±26 to 78±16 ml/min,p<0.001) and oxygen consumption in the anterior ileft ventricle and septum (11.9±4.1 to 8.4±1.9 ml 02/min,p< 0.001) in the basal state. During rapid atriial pacing, 13 of 20 patients experienced chest pain postoperatively, whereas all 20 developed chest pain during preoperative pacing, with an improvement in pacing anginal threshold (or heart rate 150 if no chest pain was experienced) of 16±18 beats/min (p <0.001). The peak great cardiac vein flow (161±41 to 131±45 mI/min, p <0.025) and myocardial oxygen consumption (19.4±6.1 to 14.3±5.5 ml 02/min,p< 0.005) during pacing, which correlated directly with the severity of the basal left ventricular gradient (p=0.011 andp=0.002, respectively), wiere also reduced by surgeryi. Lactate metabolism during pacing changed from net production before surgery to net consumption after operation (−17±47.6 to 4.4±29.8,μmol/min,p<0.01), with six of 20 patients producing lactatie after surgery compared with 13 of 20 before surgery (p=0.06). The six patients with the highest peak grieat cardiac vein flow (> 175 mVmin) during preoperative pacing had greater symptom and metabolic benefit during pacing after surgery compared with the 14 patients with lower peak coronary flow. Postpacing left ventricular end-diastolic pressure (30±7 to 23±7 mm Hg,p<0.001) and pulmonary artery wedge pressure (24±6 to 20±5,p<0.001) were reduced after surgery. Thus, operiative relief of left ventricular outflow obstruction and reduction in left ventricular systolic pressure favorably affects myocardial oxygen consumption and metabolism, due to more advantageous matching of myocardial oxygen delivery to oxygen demands during stress. The particularly marked benefit in those patients with the highest peak flow capacity before surgery may be due to less intrinsic abnormality in coronary flow delivery, perhaps due to less small vessel coronary disease, thereby favoring restoration of a more normal coronary flow reserve after surgery.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Recognition that myocardial infarction is caused by coronary thrombosis has stimulated a search for a safe, rapidly acting, and effective thrombolytic regimen. Tissue plasminogen activator (t-PA) can provide relatively clot-selective thrombolysis, but one quarter of patients fail to achieve reperfusion, lysis speed is not optimal, and higher doses have been associated with an increased incidence of hemorrhagic stroke. We report the results of a multicenter study of pro-urokinase, a second naturally occurring plasminogen activator that has structural similarities to t-PA but has a different mechanism of action. Pro-urokinase was administered 3.9±1.1 hours after the onset of chest pain to 40 patients with acute myocardial infarction with angiographically confirmed complete coronary occlusion (TIMI grade 0). After a 90-minute intravenous infusion of pro-urokinase (4.7-9 million units, 36–69 mg) 51% (20 of 39) of the patients demonstrated reperfusion (TIMI grade 2 or 3) occurring 64.8±22.3 minutes after initiation of therapy. Fibrinogen levels fell only 10±17% from baseline, confirming the fibrin specificity of pro-urokinase. As with t-PA, however, this specificity was only relative. α2- Antiplasmin decreased to 39% and plasminogen decreased to 64% of initial values. Fibrinogen degradation products increased 63% and the fibrin-specific D-dimer increased 8.7-fold. Thus, pro-urokinase produces relatively clot-selective coronary thrombolysis similar to that produced by t-PA, but the use of either pro-urokinase or t-PA alone in higher doses would be likely to produce more nonspecific effects.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The purpose of our study was to determine whether an infusion of epinephrine reverses the electrophysiologic effects of verapamil and whether reversal of verapamil's effects on the induction of paroxysmal supraventricular tachycardia (PSVT) by epinephrine during electropharmacologic testing is predictive of stress-related recurrences of PSVT during long-term treatment with verapamil. The infusion rates of epinephrine used in this study were 25 and 50 ng/kg/min, which previously have been demonstrated to result in plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. The subjects of this study were 17 patients with recurrent PSVT who underwent an electrophysiologic study in the control state and after at least 2 days of treatment with 240–480 mg/day verapamil. After assessing the response to verapamil, epinephrine was infused and testing was repeated. Verapamil significantly slowed atrioventricular conduction and prolonged refractoriness in the atrium and atrioventricular node. The effects of the two infusion rates of epinephrine were generally similar in magnitude and, therefore, the results were pooled. Epinephrine partially or completely reversed all of verapamil's electrophysiologic effects. Verapamil suppressed the induction of sustained PSVT in 15 patients. Epinephrine facilitated the induction of PSVT in seven of these 15 patients. All 15 patients were treated on a long-term basis with verapamil. The eight patients in whom epinephrine did not facilitate the induction of PSVT had no recurrences of PSVT during 9–18 months of follow-up. In contrast, there were multiple recurrences of PSVT in six of the seven patients in whom epinephrine had facilitated the induction of PSVT, and in five of these patients the episodes of PSVT occurred exclusively during exertion or emotional stress. These five patients then were treated with verapamil and 50 mg/day atenolol. Three patients could not tolerate this combination; however, the remaining two patients had no further recurrences of PSVT. In conclusion, physiologic doses of epinephrine attenuate the electrophysiologic effects of verapamil and may reverse verapamil's effects on the induction of PSVT during electropharmacologic testing. Reversal by epinephrine of verapamil's effects on the induction of PSVT may accurately identify patients who are likely to experience stressrelated recurrences of PSVT and who may benefit from treatment with a β-blocker during long-term therapy with verapamil.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The effect of preexistent coronary collateral perfusion on the prevention of left ventricular aneurysm formation was examined in 47 patients undergoing an intracoronary thrombolysis within 6 hours after the onset of a first acute anterior myocardial infarction. Left ventricular aneurysm formation and wall motion were analyzed with cineventriculography. A left ventricular aneurysm was determined as well-defined demarcation of the infarcted segment from normally contracting myocardium. In 25 patients with successful thrombolysis (group A), a left ventricular aneurysm was observed in one patient (4%) during the chronic stage of infarction. In 10 patients who had a significant collateral circulation to the infarct-related coronary artery and unsuccessful reperfusion (group B), the left ventricular aneurysm was observed in only one patient (10%). In the remaining 12 patients with unsuccessful recanalization in the absence of a significant collateral perfusion (group C), there was a higher incidence (seven of 12, 58%) of left ventricular aneurysm formation than in groups A and B (p<0.05). In group A, both the global ejection fractiion and regional wall motion in the infarct areas improved significantly (p< 0.05) between the acute and chronic stages of iinfarction. By contrast, in groups B and C, these indexes on the ventricular function did not change significantly during the convalescent period. Thus, although the collateral perfusion existing at the onset of acute myocardial infarction may not improve ventricular function, it exerts a beneficial effect on the prevention of left ventricular aneurysm formation.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Our purpose was to determine if there are basal adrenergic influences on the coronary circulation in humans. We studied 56 patients with denervated hearts after cardiac transplantation and 19 normally innervated patients with angiographically normal coronary arteries. Coronary blood flow velocity was measured during cardiac catheterization with a subselective 3F intracoronary Doppler catheter. Heart rate was controlled by atrial pacing. Epicardial coronary artery diameter was measured by automated analysis of digital coronary angiograms. Coronary flow reserve was assessed by intracoronary papaverine hydrochloride (12 mg) injections. Regional sympathetic blockade was produced by intracoronary injections of phentolamine (3 mg, α) and propranolol (2 mg, β) or metoprolol (3 mg, β1). After α-blockade, mean arterial pressure fell significantly (p<0.05) in both the denervated transplant (−5.8±1.5%) (imean±SEM) and normally innervated patients (−12.6±3.2%). Reductions in coronary flow velocity also were observed in these groups (−8.2±2.3% and −9.2±5.8%, respectively). Calculated coronary vascular resistance was unchanged. Similar changes were seen when patients were pretreated with β-blockade before α-blockade. Nonspecific β-blockade did not affect mean arterial pressure but decreased coronary velocity (innervated, −11.6±3.9% denervated, −9.3 ±2.4%) and increased coronary vascular resistance (innervated, 15.4±6.7%; denervated, 10.2±3.7%). Coronary vascular resistance did not rise in either group after selective β1-blockade with metoprolol. Coronary flow reserve did not change in either patient group after either α or βblockade. Changes in epicardial coronary artery diameter were small and generally not significant. These data suggest that α-receptor-mediated vascular tone is negligible in both denervated transplant patients and normally innervated patients. Additionally, the increase in vascular resistance after nonselective β1-blockade is the result of direct β2vascular effects. Our data further suggest that there is little adrenergically mediated epicardial artery tone (either humoral or neural) at rest and that maximal vasodilator responses are not limited by adrenergically mediated vasomotor tone.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Duplex scanning has been proposed as a safe alternative to contrast venography for diagnosing deep venous thrombosis, but its accuracy has not been proved. In this prospective, double-blind study of 47 patients, the sensitivity and specificity of duplex scan criteria were determined relative to contrast venography for lower extremity deep venous thrombosis. Criteria considered to show the presence of deep venous thrombosis included visualization of thrombus (T), absence of spontaneous flow by Doppler ultrasonography (F), absence of phasicity of flow with respiration (P), and incompressibility of the vein with probe pressure (VC). When analyzed individually, the variables T and F had low sensitivities (50% and 76%) but high specificities (92% and 100%). VC had low values for both (79% and 67%, respectively). The best single variable was P (sensitivity and specificity=92%). The best combinations of variables were T+P (sensitivity=95%, specificity= 83%), T+F+P (sensitivity= 95%, specificity=83%), F+P (sensitivity and specificity=92%), and F+T (sensitivity=92%, specificity=87%o). The low specificity of vein incompressibility was secondary to cases in which normal veins were difficult to compress in the thigh. All false-negative cases were from isolated calf vein thrombi. We conclude that isolated criteria from duplex scanning should not be used to diagnose deep venous thrombosis. In cases of suspected calf vein thrombosis, repeat duplex examination should be obtained in 3–4 days to determine the most appropriate therapy. In equivocal cases of proximal vein thrombosis, a contrast venogram should be obtained.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Vasodilation occurs in the nonexercising forearm at the beginning of isometric handgrip despite activation of sympathetic vasoconstrictor reflexes. The mechanism of this response remains unclear. In 33 normal humans, age 24±1 years (mean±SEM), we measured mean arterial pressure, heart rate, and forearm blood flow (plethysmography) in the nonexercising arm during sustained contralateral isometric handgrip at 30% maximal voluntary contraction. Sympathetic nerve activity to calf muscles (microneurography) was also measured in 15 subjects. Handgrip resulted in increases in arterial pressure from 86±2 to 97±3 mm Hg (p<0.05). Despite increases in nerve activity to calf muiscles from 229±43 to 337±66 units (p<0.005), which would be expected to produce forearmi vasoconstriction, forearm vascular resistance in the contralateral resting arm decreased from 20±3 to 18±2 units (p<0.05). To determine the mechanism of this vasodilaitory influence, additional studies were performed with regional autonomic blockade with intra-arterial administration of atropine (0.8 mg, 10 subjects) or propranolol (2.0 mg, eight subjects) into the nonexercising forearm before contraction. Propranolol and vehicle had no effect on forearm vascular responses in the resting arm during SHG in the other arm. In contrast, atropine blocked the vasodilatory response in the resting arm during contraction (A forearm vascular resistance during contraction, control= −2.1±0.6 units; postatropine= +0.2±0.9 units,p<0.05). Atropine did not attenuate the vasodiilator response to isoproterenol or the vasoconstrictor response to norepinephrine. We conclude 1) a dissociation exists between sympathetic neural and forearm vascular responses to isometric exercise; 2) the vasodilatory response in the nonexercising forearm is not due to sympathetic withdrawal or β2-adrenergic-mediated vasodilation; and 3) this response is mediated primarily by cholinergic mechanisms. These studies provide the first direct evidence for active, cholinergically mediated vasodilation during exercise in humans.

ISSN:0009-7322    

出版商:OVID    

年代:1989

数据来源: OVID