Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ventriculograms made 9-15 months after surgery in 48 patients with normal preoperative apical contraction were reviewed to determine the influence of apical venting on apical wall motion in patients undergoing coronary bypass surgery. After interpretation of postoperative apical wall motion, the patients were subdivided into two groups. One group consisted of 34 patients who were vented by inserting a catheter through the apex of the left ventricle and the second group included 14 patients in whom no transventricular vent was made. The two groups were similar clinically and hemodynamically before surgery, and the surgical procedures were similar with the exception of vent site. Following surgery, incidences of graft patency and antegrade flow to the apex were also similar. Nineteen (56%) patients in the apically vented group had apical dyskinesia or akinesia observed on the postoperative ventriculogram while none of the patients who were not apically vented had these findings. None of the patients with apical dyskinesia or akinesia had congestive heart failure following surgery. The postoperative ventriculograms of 12 patients with mitral stenosis who underwent valvulotomy by inserting a Tubbs dilator through the apex were also analyzed. Only one patient (8.5%) had apical dyskinesia or akinesia. Since the patients with mitral stenosis probably did not have significant coronary artery disease, it is possible that the combination of the apical vent and ischemic heart disease was responsible for the focal contraction abnormalities observed.
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PMID:Ventricular apical vents and postoperative focal contraction abnormalities in patients undergoing coronary artery bypass surgery. 30 45

In order to study factors influencing posterior wall thickness during diastole, echocardiograms showing the septum, mitral valve and posterior wall endocardium and epicardium in 15 normal subjects and 49 patients with heart disease were digitized. Maximum wall thickness, minimum cavity dimension and the onset of mitral valve opening are normally synchronous, and an early period of rapid wall thinning, at a peak rate of 10.7 +/- 1.7 cm/sec corresponds closely to rapid filling. In patients with ischaemic heart disease the peak rate and duration of rapid thinning were normal, but thinning preceded mitral valve opening (mean 50 msec). In 11 of 17 patients with hypertrophic cardiomyopathy the peak rate of thinning was reduced and in 2 it was increased. There was a close correlation between the peak thinning rate in this group and the peak rate of increase in dimension. In mitral stenosis peak thinning rate was frequently reduced but in some patients was normal, with the reduced rate of increase in cavity dimension maintained by reversal of septal movement. We conclude that rapid thinning is an intrinsic property of the ventricular wall which is normally associated with rapid filling, but which may be dissociated from filling by asynchronous relaxation or inflow obstruction, or may be modified by myocardial disease.
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PMID:Diastolic changes in left ventricular wall thickness studied by echocardiography. 41 5

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P less than 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P less than 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P less than 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.
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PMID:Right ventricular diastolic pressure in coronary artery disease. 50 30

The left ventricular systolic ejection phase was cineangiographically analyzed in an attempt to evaluate left ventricular performance. Forty-eight patients were classified into five groups: (1) 9 controls; (2) 5 patients with PMD (congestive type) (COCM); (3) 9 patients with PMD hypertrophic type) (HCM), (4) 9 patients with ischemic heart disease (IHD); and (5) 16 patients with mitral stenosis (MS). The rate of volume change (deltaV/deltat) and the volume change as a percentage of stroke volume (deltaV/SV) in patients with COCM and IHD were lower in the early systole and higher in the mid-systole as compared with the control group. Normalized systolic ejection rate (NSER) and velocity of circumferential fiber shortening (Vcf) for the early and late systole were significantly lower in patients with COCM and IHD than in the control group. In two patients with IHD in whom normal indices of left ventricular performance and no asynergy were observed, NSER and Vcf were normal in the late systole but were significantly lower in the early systole. In all 48 patients, deltaV/deltat, deltaV/SV, NSER and Vcf were compared statistically with conventional ejection phase indices and isometric phase indices. delthV/SV for the midstystole showed a negative correlation with EF, MNSER and mVcf. NSER and Vcf for all three phases showed a good correlation with Vmax, max dp/dt and R-max dp/dt but a better correlation with EF, MNSER and mVcf. It was concluded that NSER and Vcf for the early systole were sensitive indices of left ventricular performance and may be utilized to detect subtle depression of left ventricular performance.
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PMID:Quantitative analysis of left ventricular ejection phase by means of left ventricular cineangiography. 59 71

The one-pole peripheral AVR lead reflects the changes in the electromotive power of the heart in a frontal plane in a reverse (mirror) image. In 620 subjects with healthy hearts, with the aid of an extended ECG method; the variants of the auricle-ventricle complex in AVR lead in norm and the separate heart positions, were studied. The pathologically changed P-wave was established to be presented by its typical forms (P-mitrale, P-pulmonale), but in a mirror image in AVR lead. The positive auricle wave in AVR is an important sign for the presence of right-auricular ectopic rhythm. In 80 patients with left-ventricular loading, pathologically enlarged S deflection was found. In 232 patients with fight-ventricular loading (mitral stenosis, chronic pulmonary heart), the increase of the amplitude of the deflection R AVR and the change in the ratio R/Q aVR over 1, is a valuable information about the degree of the right-ventricular loading. Those changes closely correlate with the changes in the ventricular complex with the right thoracic leads and with the spirographic and X-ray examinations. the role of AVR lend in the differential diagnostic determination of the additional deflection r'R'aVR1 V1 in certain forms of disturbed intraventricular conductivity is emphasized. AVR lead reacts dynamically with the separate sites of myocardial necrosis, with the appearance of unusual forms of the ventricular complex in AVR (increased first R deflection AVR in posterior-inferior myocardial infarction, occurence of rSr' forms in AvR in posterior-basal infarction and wide split ventricular complexes in anterior (anteriorseptal)infarction, complicated with a bundle blockade. Myocardial ischemia (subpericardial and subendocardial) is represented in A V R in an image reverse to the left thoracic leads. A general conclusion is drawn that the separate interpretation of the changes in AVR lead is not reasonable. Its differential diagnostic value grows only with its synchronic analysis with the rest peripheral and especially precordial leads.
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PMID:[Differential diagnostic value of the aVR lead]. 73 34

Employing a new catheter and technique complete retrograde left heart catheterization was accomplished in 96 of 100 consecutive patients. These 96 patients included 37 with ischemic heart disease, 13 of 17 with isolated aortic valve deformities, 11 with isolated rheumatic mitral valve deformities, 10 with combined rheumatic aortic and mitral valve deformities, and 25 with other problems. The only failures were in 4(of 27) patients with aortic valve deformities. No untoward complications occurred. The retrograde catheterization fluoroscopy time was usually less than 2 minutes. The shortest time was 44 seconds, the longest, 6 minutes and 2 seconds. These data indicate that this new catheterization method achieves safe, reliable (when the aortic valve is not deformed), simple, and rapid complete left heart catheterization. They further indicate it may be useful in assessing patients with mitral stenosis, pulmonary hypertension, hypertrophic obstructive cardiomyopathy, and left-to-right shunt problems.
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PMID:New performed catheter and method for retrograde left atrial or complete left heart catheterization. 73 34

The left ventricular end-diastolic volume (EDV), end-systolic volume (ESV) and systolic ejection fraction (SV/EDV) were determined in 6 healthy subjects, 21 patients with ischemic heart disease and 8 patients with mitral stenosis by the left ventricular 133Xe washout technique. Cardiac and stroke indexes as well as left ventricular work and stroke work indexes do not differ in all three groups. A significantly higher EDV and ESV together with a low SV/EDV suggested impaired left ventricular function in patients with ischemic heart disease.
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PMID:Left ventricular end-diastolic volume in advanced ischemic heart disease; comparison between healthy subjects and patients with mitral stenosis. 118 18

A 58-year-old woman, referred to our hospital to undergo invasive assessment of mitral valve stenosis, demonstrated prolonged asymptomatic catheter-induced left anterior descending and right coronary artery spasm during coronary arteriography. Coronary spasms were not associated with ECG and arterial blood pressure changes. Intracoronary injection of nitroglycerin (300 and 600 micrograms bolus) did not resolve coronary spasm. Coronary angiography, repeated 24 hours later using the same procedure and materials, did not show any evidence of coronary artery spasm. The present clinical case is interesting for 3 reasons. First, the presence of prolonged proximal double-vessel coronary spasm not associated with symptoms or signs of acute myocardial ischemia; second, the incapacity of high dose of intracoronary nitroglycerin to resolve the coronary spasm; third, the dramatic changes in the sensitivity of coronary artery to mechanical stimulation in different days.
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PMID:Prolonged asymptomatic catheter-induced left and right coronary artery spasm resistant to high dose of intracoronary nitroglycerin. 129 76

A consecutive series of 1288 mitral valves surgically excised from 1981 through 1989 were studied macroscopically and histologically. The explanted valves were affected by: chronic rheumatic disease (1179, 91.5%), floppy mitral valve (84, 6.5%), bacterial endocarditis (19, 1.5%), and post-ischemic mitral incompetence (6, 0.5%). Among 1179 post-rheumatic cases, mixed mitral stenosis and incompetence was the most frequent malfunction (747, 58%). Isolated mitral incompetence was diagnosed in 72 (6.11%) cases only, and isolated stenosis in 360 cases. In 52 valves, excised because of chronic rheumatic disease, the histology showed unexpected signs of acute rheumatism of the leaflets and the papillary muscles. In these patients clinical symptoms and blood tests were negative for rheumatic disease. Mitral incompetence, possibly due to papillary muscle dysfunction, was the prevalent lesion (61.5%). A total of 181 patients (14.05%) with pure mitral incompetence underwent surgery. In 84 patients (46.4%), the floppy mitral valve was the most frequent cause of valve dysfunction, 72 (39.8%) had rheumatic disease, 19 (10.5%) infective endocarditis, and 6 (3.4%) ischemic heart disease. In the group with floppy mitral valve, males were more prevalent than females (51:33). The mean age of the 4 patients with Marfan's syndrome and non-Marfan patients was noticeably different (17 vs 49 yr). Moreover leaflet deformation, tendinous cord elongation and annulus dilatation were the most common causes of valve incompetence. Floppy mitral valve and infective endocarditis were the cause of cordal rupture in 43.5% of the cases. This was a severe complication which always required emergency surgery.
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PMID:Surgical pathology of the mitral valve: gross and histological study of 1288 surgically excised valves. 142 93

From a very heterogeneous group of 340 patients undergoing mitral valve reconstruction from 1969 through 1988, 313 hospital survivors were analyzed for factors affecting the occurrence of reoperative mitral valve procedures related to native mitral valve dysfunction. Follow-up was 100% and extended from 1 year to 20 years (mean follow-up, 7.2 years). Sixty-three patients (18.5% of the 340) required mitral valve reoperation at a mean postoperative interval of 6 years (range, 1 to 15 years). Incremental risk factors analyzed for the event late mitral valve failure included age, sex, preoperative New York Heart Association class, cause of valvular disease, pathophysiology of the mitral valve, previous mitral valve operation, mitral valve pathology, and estimation of mitral valve function at operation after repair. Mitral valve pathophysiology affected the actuarial freedom from mitral valve replacement (p = 0.023 [log-rank]). Actuarial freedom from mitral valve reoperation was 90% at 5 years and 80% at 8 years in patients who had either pure mitral regurgitation or isolated mitral stenosis compared with 80% and 72% at 5 and 10 years, respectively, in patients who had mixed mitral stenosis and regurgitation (p = 0.023). Patients undergoing late reoperation were younger (51.7 +/- 1.56 years [+/- the standard error of the mean]) than those not having reoperation (p less than 0.0003). Durability of the repair was less in patients with rheumatic heart disease (p less than 0.025) and greater in patients with ischemic heart disease (p less than 0.004). Seventy-three percent of patients undergoing reoperation had concomitant operations compared with 68% of those not having reoperation (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors affecting mitral valve reoperation in 317 survivors after mitral valve reconstruction. 151 May 10


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