ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT To quantitate the amount of right and left ventricular infarction in patients dying with postinfarction ventricular septal defect (PIVSD), hearts from 54 patients with anterior or inferior myocardial infarction were studied at autopsy. Fifteen hearts had myocardial infarction with PIVSD and 39 hearts had infarction without PIVSD and were used as a comparison group. All infarcts were sized histologically and the percent of each ventricle infarcted was quantitated by computer-assisted planimetry. The pathologic substrate for PIVSD was diffuse coronary artery disease with acute thrombosis resulting in transmural confluent infarction. Within the PIVSD group, there was significantly more left ventricle involved in anterior infarctions than in inferior infarctions (p<.04). Conversely, there was more right ventricular infarction in inferiorly located myocardial infarctions with resulting PIVSD (p = .059). When infarctions resulting in PIVSD were compared with infarctions not resulting in PIVSD, the PIVSD group was characterized by larger left and right ventricular infarcts irrespective of infarct location (p<.003). The incidence of right ventricular infarction was 100% in the PIVSD group (p<.0001). Twelve of the 15 patients with PIVSD (80%) developed cardiogenic shock within 48 hr of septal rupture. The high incidence of shock and the rapid deterioration may have been secondary to right ventricular infarction in these patients. Therefore, infarcts resulting in PIVSD and subsequent death are characterized by a high incidence of right ventricular infarction. Significantly more infarction of the right ventricle is seen in either anterior or inferior infarctions resulting in PIVSD compared with infarctions not resulting in PIVSD. PIVSD complicating inferior infarctions is associated with the greatest amount of right ventricular infarction.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Increased vascular constriction has been observed at the site of atherosclerotic lesions, suggesting an association between atherosclerosis and altered vascular tone. While atherosclerosis may increase sensitivity to exogenous vasoconstrictors, little is known about the response of normal and atherosclerotic coronary arteries to an exogenous stimulus that excites the sympathetic nervous system. Therefore, we studied the response to cold pressor test (CPT) using quantitative angiography and Doppler flow velocity measurements in eight patients with angiographically normal coronary arteries (group I), nine patients with mild coronary atherosclerosis (< 50% diameter narrowing) (group II), and 13 patients with advanced coronary stenoses (> 50% diameter narrowing) (group III). In 31 segments of angiographically smooth arteries in group I, the CPT produced vasodilation from a control mean diameter of 2.68 ± 0.09 (mean ± SE) to 2.99 ± 0.09 mm at peak CPT (p < 0.001), a 12 ± 1 % increase in diameter. In group II, 27 irregular segments constricted to peak CPT from a mean control diameter of 1.82 ± 0.12 to 1.66 ± 0.12mm (p< .001), a 9 ± 1%decrease, while 10 smooth segments dilated from a mean control diameter of 1.98 ± 0.11 mm to 2.34 ± 0.15 mm (p < .01), a 19 ± 2% increase in diameter. Likewise, in group III, the 17 stenotic segments constricted from 1.16 ± 0.09 to 0.89 ± 0.09 mm (p < .001), a 24 ± 6% decrease; the irregular segments also constricted from 2.44 ± 0.11 to 2.22 ± 0.12 mm (p = .002), a 10 ± 2% decrease. In contrast, two smooth segments dilated from 2.98 to 3.23 mm (mean), an 8% increase in diameter. Coronary blood flow increased 65 ± 4% (mean) during CPT in group I, it increased 15 ± 6% in group II, and it decreased 39 ± 8% in group III. The vasodilator response in four normal patients was partly inhibited by the administration of intracoronary propranolol (17 ± 3% increase during control, 10 ± 2% increase after propranolol, 41% less dilation; p = .002). We conclude that the response of normal coronary arteries to the CPT test is dilation, in part related to β-adrenoreceptor stimulation and possibly flow-mediated endothelial dilation or α2-adrenergic activity. The paradoxical vasoconstrictor response induced by atherosclerosis may represent altered catecholamine sensitivity and/or a defect in endothelial vasodilator function. The presence of atherosclerosis impairs vasodilator responses and thus may contribute to the pathogenesis of myocardial ischemia.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

We examined the relationship between blood pressure and dietary sodium and potassium intake estimated from 24 hr diet recall in a population of 584 men and 718 women 30 to 79 years old in Southern California. In men, but not women, age-adjusted systolic and diastolic blood pressure correlated significantly with dietary sodium intake. In both men and women, age-adjusted diastolic blood pressure significantly inversely correlated with dietary potassium intake. Age-adjusted systolic and diastolic blood pressure correlated significantly with the dietary sodium/potassium ratio in each sex; correlations were better for the ratio than for either sodium or potassium alone. The relationship was apparent over the whole range of blood pressure and dietary intake. A marked age gradient was apparent in men, the regression slope for blood pressure vs sodium/potassium ratio increasing with increasing age, suggesting increasing sensitivity to dietary sodium/potassium ratio with age. Adjusting for intake of other dietary variables, including calories, protein, carbohydrate, saturated fat, alcohol, calcium, and fiber, did not alter the relationships; adjusting for body mass index reduced the strength of the association in women but not in men. These results support the hypothesis that dietary sodium and potassium are related to blood pressure within a population.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

With the use of biplane selective ventriculography, the ventricular volume, ejection fraction, and ventricular mass were evaluated in 28 patients with a single ventricle, and those with the left ventricular type (LV type, 12 patients) and right ventricular type (RV type, 16 patients) were compared. There were no significant differences in terms of age, hemoglobin, systemic oxygen saturation, or pulmonary-to-systemic flow ratio in the two groups. No patients with atrioventricular valve regurgitation were included. The ventricular cavity volume was calculated by the area-length method. The ventricular mass volume was determined as the shell volume created by subtracting the ventricular cavity volume from the total ventricular volume calculated by adding the free wall thickness to the chamber dimensions. The ventricular mass volume was converted to mass by multiplying by the gravity of the heart muscle. There was no significant difference between patients with the LV type and RV type of single ventricle with respect to the end-diastolic ventricular volume (188 ± 53 and 179 ± 61 ml/m2 in LV and RV types, respectively), end-systolic volume (88 ± 31 and 84 ± 27ml/m2), or ejection fraction (0.54 ± 0.06 and 0.52 ± 0.06). The following four indexes of the ventricular mass were significantly (p < .001) lower in patients with the RV type of single ventricle: ventricular wall thickness (3.9 ± 1.2 mm in RV type vs 6.9 ± 1.9 mm in LV type), ratio of the ventricular wall thickness to the transverse diameter of the ventricle (6.8 ± 1.9% vs 12.1 ± 2.4%), ventricular mass (87 ± 35 vs 160 ± 47 g/m2), and ratio of ventricular mass to end-diastolic volume (0.48 ± 0.11 vs 0.88 ± 0.17 g/ml). There was a positive linear correlation between the ventricular mass index and the pulmonary-to-systemic blood flow ratio in patients with LV type (r = .71, p < .01) but no correlation was seen in those with RV type. These results suggest that there is inadequate ventricular hypertrophy (insufficient ventricular mass to ventricular volume) in patients with the RV type of single ventricle compared with that in those with the LV type and this may lead to abnormal contractile state and poor adaptation of ventricular function in patients with the RV type of single ventricle.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Alterations in ventricular loading conditions lead to changes in action potential duration and arrhythmias via contraction-excitation feedback; a decrease in load leads to prolongation of repolarization. To determine whether changes in right ventricular load alter ventricular repolarization in man, the corrected QT interval, a measure of overall ventricular repolarization, was measured in 32 patients before and after valvuloplasty for pulmonary stenosis. Right ventricular systolic pressure decreased (82.5 ± 30.7 to 40.5 ± 9.5 mm Hg, p<.001) and the QTC increased concurrently (409.1 ± 24.3 to 440.7 ± 28.0 msec, p<.001) after successful valvuloplasty. The increase in QTC was most marked for those patients with a greater than 30 mm Hg decrease in right ventricular pressure (40.0 ± 22.3 vs 16.3 ± 21.3 msec, p = .006). In a subset of seven patients in whom monophasic action potentials were recorded, monophasic action potential duration, a measure of local repolarization, was prolonged (230.0 ± 24.3 vs 216.9 ± 21.9, p<.001) after successful valvuloplasty, confirming that the QTC prolongation reflected changes in local ventricular repolarization. In addition, during nine acute right ventricular outflc w tract occlusions in a subset of six patients, monophasic action potential duration shortened (206.6 ± 17.6 vs 221.7 ± 20.9 msec, p<.01) and early afterdepolarizations developed consistent with contraction-excitation feedback. These data suggest that, in humans, changes in mechanical load are associated with changes in ventricular repolarization consistent with contraction-excitation feedback.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Two Doppler methods, the pressure half-time method proposed by Hatle and the method based on the equation of continuity, were used to estimate stenotic mitral valve area noninvasively, and the accuracy of these methods was examined in patients with and without associated aortic regurgitation. Mitral valve area determined at catheterization by the Gorlin formula was used as a standard of reference. The study population consisted of 41 patients with mitral stenosis, and 20 of the 41 patients had associated aortic regurgitation. According to the equation of continuity, mitral valve area was determined as a product of aortic or pulmonic annular cross-sectional area and the ratio of time velocity integral of aortic or pulmonic flow to that of the mitral stenotic jet. Mitral valve area was determined by the pressure half-time method as 220/pressure half-time, the time from the peak transmitral velocity to one-half the square root of the peak velocity on the continuous-wave Doppler-determined transmitral flow velocity pattern. The pressure half-time method tended to overestimate catheterization measurements, and the correlation coefficient for this relation was .69 (SEE = 0.44 cm2). The correlation coefficient improved to .90 when the patients with associated aortic regurgitation were excluded. Mitral valve areas determined by the continuity equation method correlated well with catheterization measurements at a correlation coefficient of .91 (SEE = 0.24 cm2), irrespective of the presence of aortic regurgitation. The ratio of the time-velocity integral of aortic or pulmonic flow to the time-velocity integral of mitral stenotic jet also correlated well with mitral valve area determined by catheterization at a correlation coefficient of .84 (SEE = 0.10). Thus we conclude that the pressure half-time method produces a significant overestimation of mitral valve area in patients with associated moderate-to-severe aortic regurgitation and that in such cases the continuity equation method should be used to quantify mitral valve area noninvasively. The simplified continuity equation method also provides an accurate estimate of mitral valve area with few limitations.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

To characterize the sequential changes of myocardial perfusion scintigraphy in patients with coronary artery disease (CAD) after complete revascularization, 43 patients underwent exercise thallium-201 (201T1) myocardial perfusion scintigraphy before and at 9 ± 5 days, 3.3 ± 0.6, and 6.8 ± 1.2 months after percutaneous transluminal coronary angioplasty (PTCA). Only patients with single-vessel CAD, without previous myocardial infarction, and without evidence of restenosis at 6 to 9 months after PTCA were included. Perfusion scans were analyzed blindly with the use of a new quantitative method to define regional myocardial perfusion in the topographic distribution of each coronary artery, which was shown to be reproducible (r = .94 or higher and SEE of 7% or less, between repeated measures by one and two operators). At 4 to 18 days after PTCA, the mean treadmill walking time increased by 123 ± 42 sec, mean exercise-induced ST segment depression decreased by 0.6 ± 0.3 mm, group maximal heart rate increased by 20 ± 9 beats/min, and group systolic blood pressure at peak exercise increased by 24 ± 10 mm Hg, compared with pre-PTCA values (p < .001). However, no group differences were noted in these variables between the three post-PTCA stages. Myocardial perfusion in the distribution of the affected (dilated) coronary artery, on the other hand, improved progressively. In the 45 degree left anterior oblique view for instance, myocardial perfusion increased at 9 days after PTCA (from 68 ± 24% before PTCA to 91 ± 9%, p < .001) and at 3.3 months after PTCA (101 ± 8%, p < .05 vs 9 days after PTCA), but no further significant changes were seen at 6.8 months after PTCA (102 ± 8%). Similar changes were noted in the other two views. No relationship between minor complications during PTCA and delayed improvement on the 201T1 was observed. Myocardial ischemia was diagnosed in 12 of the 43 scans recorded a few days after PTCA, but in none recorded at later stages. We conclude that 201T1 scans after PTCA often show delayed improvement and therefore, an abnormal myocardial perfusion scan soon after PTCA does not necessarily reflect residual coronary stenosis or recurrence.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID