Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 206 consecutive patients having undergone mitral valve repair with a prosthetic ring between 1972 and 1979 in our institution, the 195 patients (94.5%) who survived the operation were studied to assess the long-term function of this method of repair. Patients' ages ranged from 18 to 79 years (mean age 48.7 years). Mitral valve insufficiency was due to degenerative disease in 113 patients (58%), rheumatic disease in 74 (38%), ischemia and other causes in eight patients (4%). A total of 188 patients (9.7%) were in New York Heart Association class III or IV preoperatively and 94 (48%) had atrial fibrillation. The patients were divided into three functional groups: type I (normal leaflet motion), 35 patients (18%); type II (leaflet prolapse), 147 patients (75%); and type III (restricted leaflet motion), 13 patients (7%). The techniques included prosthetic ring annuloplasty (185 patients), leaflet resection (158 patients), chordal shortening (89 patients), leaflet mobilization (10 patients) and papillary muscle reimplantation (2 patients). Long-term follow-up was available in 189 patients (96.8%), for a rate of 2316 patients per year. The 15-year actuarial and valve-related survival rates were 72.4% and 82.8%, respectively. At 15 years, 93.9% of the patients were free from thromboembolism, 96.6% free from endocarditis, 95.6% free from anticoagulant-related hemorrhage, and 87.38% free from reoperation. Actuarial rate of freedom from reoperation was higher in the group with degenerative disease (92.7%) than in the group with rheumatic disease (76.12%). Among the 157 survivors, 117 (74%) were in New York Heart Association class I and class II and 105 (66%) were in sinus rhythm. Doppler echocardiographic studies showed normal ventricular contractility in 134 patients (84.5%), absence of mitral regurgitation in 112 (74%), trivial regurgitation in 27 (17%), and significant regurgitation in 4 patients (2.5%).
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PMID:Valve repair with Carpentier techniques. The second decade. 235 39

To elucidate the incidence and natural history of valvular heart disease in Kawasaki syndrome, we analyzed patients who were found to have a new heart murmur after the onset of the disease. Among 1215 patients we found 13 (1.1%) with valvular disease (12 with mitral regurgitation and one with aortic regurgitation). We compared these patients with 30 who did not have valvular lesions. The duration of fever was longer and the incidence of coronary artery lesions significantly higher than in those without valvular disease. Heart murmurs disappeared within 2 months after the onset of valvular heart disease in five patients, whereas in another six, all involving valve prolapse, they persisted for 2 years or more. We postulate that two different mechanisms may be responsible for the variation in the duration of valvular heart disease: one, which disappeared spontaneously, was attributed to pancarditis; the other, which persisted, was due to dysfunction in valve and papillary muscles as a result of ischemia.
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PMID:Valvular heart disease in Kawasaki syndrome: incidence and natural history. 238 13

The examination of a patient with angina pectoris begins with clinical assessment. Certain clinical findings that are present only during angina, such as mitral regurgitation due to ischemia-induced papillary muscle dysfunction, may clarify an otherwise uncertain diagnosis. Electrocardiography is a useful and relatively inexpensive test for detecting evidence of ischemia in patients with suspected angina. The presence of cardiomegaly on the chest roentgenogram has adverse prognostic implications. Exercise stress testing is important in the diagnosis of coronary artery disease and also provides prognostic information. Patients should be classified into high-, intermediate-, or low-risk subsets by noninvasive techniques. Although relatively easy and inexpensive, treadmill exercise stress testing cannot be performed in all patients, and sometimes it will yield equivocal results. In these cases, radionuclide testing (with thallium scintigraphy or radionuclide angiography) can be helpful and also can identify high-risk patients. Some patients will require coronary angiography.
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PMID:Stable angina pectoris: 2. Cardiac evaluation and diagnostic testing. 240 23

To evaluate left ventricular diastolic function during dipyridamole-provoked myocardial ischemia, transmitral flow was studied in 73 patients with coronary artery disease and 8 normal subjects using pulsed Doppler echocardiography. Coronary vasodilating agents like dipyridamole can provoke myocardial ischemia in patients with coronary artery disease. The peak flow velocity of left ventricular rapid filling (R), that of atrial contraction (A) and the ratio of A to R (A/R) in each cardiac cycle were measured. The rapid filling phase was divided into two subphases at the point of R. The integral of the two subphases and atrial contraction were computed and designated IR1, IR2 and IA. The time intervals of the two subphases of rapid filling were designated TR1 and TR2. Of the 73 patients with coronary artery disease, 41 patients developed ischemia (positive responder = PR) and 32 patients did not (negative responder = NR) after dipyridamole infusion. In PR, A/R increased (p less than 0.05), IR2 decreased (p less than 0.01) and TR2 shortened (p less than 0.01) significantly. In NR and normal subjects, these indices remained unchanged. We observed mitral regurgitation (MR) in 13 PR patients during acute myocardial ischemia. A/R increased in patients without MR but A/R remained unchanged in patients with MR. These results suggest that in acute myocardial ischemia, changes in Doppler indices (A/R, IR2 and TR2) reflect a left ventricular diastolic abnormality, and that the masking of the diastolic abnormality was ascribed to the presence of MR.
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PMID:Noninvasive assessment of left ventricular diastolic filling in coronary artery disease by Doppler dipyridamole-stress testing. 263 30

Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic entity that involves principally the left ventricle and is caused by asymmetric or concentric hypertrophy of unknown cause. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the apex, at the midventricular level, or, rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by upper septal hypertrophy narrowing the outflow tract and setting the stage for Venturi forces to cause systolic anterior motion of the anterior or posterior mitral leaflets. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyotomy-myectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. This form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy available today. The extent of hypertrophy is believed to be the principal determinant of the impaired left ventricular relaxation and increased chambers stiffness (decreased compliance) that characterize diastole in hypertrophic cardiomyopathy. Relaxation is impaired by the contraction load (the obstruction), by a decrease in the principal relaxation loads, by a pathologic degree of nonuniformity of contraction and relaxation, and in all likelihood, by impaired inactivation of the biochemical processes responsible for contraction (? due to primary or ischemia-induced calcium overload). Calcium channel-blocking agents may dramatically improve left ventricular relaxation by speeding up the inactivation process, by decreasing the degree of nonuniformity, or by altering the contraction and relaxation loads in a favorable manner. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their occurrence also appears to depend on the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole as well as the disturbances of rhythm appear to be related to the site and/or extent of the hypertrophic process.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertrophic cardiomyopathy. The importance of the site and the extent of hypertrophy. A review. 316 67

Mitral regurgitation (MR) reportedly develops by ischemia of the papillary muscles, which is called papillary muscle dysfunction. This report deals with the roles of papillary muscles and left ventricular walls on the pathogenesis of MR using graded injuries of these structures in 23 dogs. Implanted ultrasonic microcrystal and occluder with an electromagnetic flowmetry for the left circumflex coronary artery were the main experimental setting. Graded occlusion of the artery was done by the six-step approach regarding coronary blood flow (CBF) reduction (C1-C6). Left ventricular (LV) pressure, systolic thickening (%W: sonomicrometry) of the LV anterior (AW) and posterior walls (PW), and systolic longitudinal shortening (%S: sonomicrometry) of both the anterior and posterior papillary muscles (PPM) were measured. MR was assessed by left ventricular contrast two-dimensional echocardiography. In eight dogs, all the data were adequate for analysis. In category 3 (C3: 55-70% CBF of control), %S in PPM decreased, but %W did not change significantly, and only mild MR developed in three of the eight dogs. MR clearly developed in category 4 (C4: 40-54% CBF as compared with the control stage), where %S was replaced by holosystolic lengthening and %W reduced to 50% of the control state, and total occlusion (C6) accompanied by significant thinning of both the PW and AW. Thus, the asynergy of the LVPW was needed to induce the MR in seven of the eight dogs. It was concluded that the injury of the PPM alone is not sufficient to cause MR, and the associated ischemic changes of the LV free wall as well as LV dilatation are necessary to induce severe MR.
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PMID:[Experimental mitral regurgitation in ischemia-induced papillary muscle dysfunction]. 325 3

Mitral valve repair has been increasingly used at our hospital for mitral regurgitation with and without coronary disease. From January, 1984, to June, 1987, of 338 patients undergoing all forms of mitral valve surgery, 140 had first-time surgery for pure mitral regurgitation: 75 had valve repair, and 65 had valve replacement. Thirty-three of 75 (44%) had concomitant coronary bypass in the repair group, while 21 of 65 (32%) had coronary bypass in the replacement group. The mean functional class (3.4 versus 3.5), age (60 versus 61 years), and preoperative hemodynamics were similar in both groups. The cause of mitral regurgitation in the repair group was myxomatous change in 32 patients, ischemia in 27, rheumatic valve disease in 12, and endocarditis in 4. A Carpentier ring was used in 46, a Duran ring was used in 11, and none was used in 18. The operative mortality was 3 of 75 patients (4%) in the repair group, all with coronary artery bypass grafting, versus 2 of 65 patients (3%) in the replacement group, 1 of whom had undergone coronary artery bypass grafting. The mean postoperative functional class 15 months postoperatively was 1.12 in the repair group versus 1.15 in the replacement group. There were 7 late deaths in the replacement group and only 3 late deaths in the repair group. Actuarial survival at 30 months was 85 +/- 6% for the replacement group and 94 +/- 4% for the repair group. There were 5 late emboli (1 fatal, 4 nonfatal) after valve replacement and none after valve repair (p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative morbidity of mitral valve repair versus replacement for mitral regurgitation with and without coronary artery disease. 325 47

The role of coronary artery bypass (CAB) surgery in patients with recent myocardial infarction remains controversial. To more clearly define the operative risks, we reviewed 336 patients who underwent isolated CAB within 30 days of infarction. There were 129 patients with stable or no angina (Group 1), 163 with angina at rest (Group 2), 21 with angina requiring intra-aortic balloon counterpulsation for pain control (Group 3), and 23 with severe postinfarction ischemia or extension complicated by cardiogenic shock (Group 4). There were 26 (7.7%) deaths overall. The mortality was 2.3% in Group 1, 6.1% in Group 2, 9.5% in Group 3, and 47.8% in Group 4. Univariate analysis (Student's t and chi 2 tests) and multivariate analysis (stepwise logistic regression model) were performed on 17 variables: age, gender, clinical Group (1-4), number of diseased vessels, presence of left main artery disease, left ventricular wall-motion score, left ventricular end-diastolic pressure, presence of mitral insufficiency, extent of infarction (subendocardial vs. transmural), interval from infarction to CAB, number of distal anastomoses performed, preoperative hemodynamic status, aortic cross-clamp time, and total cardiopulmonary bypass time. Only advanced age (p = 0.002), left ventricular wall-motion score (p = 0.004), and clinical group (p = 0.048) proved to be independent predictors of mortality by multivariate analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary artery bypass for recent infarction. Predictors of mortality. 326 48

The clinical characteristics and prognosis of 16 cases of mitral regurgitation (MR) secondary to Kawasaki disease (KD) were studied, and its pathogenesis was discussed. The observation period ranged from 3 years and 17 months to 15 years. Six of the 16 patients died, and 10 are alive. MR has disappeared spontaneously in 2 of these survivors. Thirteen of the 16 patients were male and 3 were female, there being a predominance in male, which is a striking contrast to rheumatic mitral regurgitation which is predominant in females. The age at the time of diagnosis ranged from 3 months to 7 years. The appearance time of MR showed two different patterns, one with early onset within a few weeks to one month after affliction with KD and the other with MR developing months or years later during the course of the follow-up. The cardiothoracic ratio was greater in those who had a progressively downhill course, and whose sigma RV1-6 decreased with time course. This was considered to be due to the decrease of the remaining functioning myocardial mass. The outcome of the patients with a severe degree of coronary arterial stenosis and occlusion observed on the coronary angiogram was poor. The prognosis of the patients with severe left coronary arterial stenosis was especially poor. MR due to KD is regarded as a new clinical entity, and its pathogenesis is thought to be due to ischemia, papillary muscle dysfunction, coronary angitis, myocardial failure and valvulitis. Incidence of MR will increase when examined by Doppler echocardiography especially in the acute stage. Our experience as well as that of others indicates the presence of valvulitis, myocarditis or left ventricular dilatation leading to MR in the acute stage.
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PMID:Mitral regurgitation in Kawasaki disease. 342 45

Determination of the optimal time for surgical intervention in chronic mitral regurgitation has remained controversial. There are similarly important factors in favor of temporizing with medical treatment alone as there are in support of relatively early surgery (Table 1). Since rheumatic valvulitis may play a subordinate role, in contrast to etiologies such as myxomatous degeneration of the mitral valve, rupture of chordae tendineae, papillary muscle dysfunction due to coronary artery disease and other causes, left ventricular function is generally determined by the adaptations of the myocardium to the volume overload, or to ischemia or infarction from coronary artery disease rather than to a concomitant myocarditis. Based on actuarial survival curves in symptomatic patients with combined mitral regurgitation and stenosis or mitral regurgitation alone, it can be assumed that surgery can result in improved survival, in particular if a reconstructive mitral valve procedure rather than prosthetic valve replacement is performed. Medical treatment is carried out with digitalis to enhance myocardial contractility, diuretics and vasodilators to reduce pre- and afterload with resultant diminished effective mitral orifice area and regurgitant volume, lowering of pulmonary artery and pulmonary venous pressures and an increase in systemic cardiac output. Presently, however, there is no convincing evidence that symptom-status is improved or the natural history favorably affected over a number of years. For assessment of left ventricular myocardial function the end-systolic pressure/volume or the end-systolic stress/volume index appear preferable. Values of the latter less than or equal to 2.2 are associated with increased postoperative mortality and improbable improvement in functional status. Additionally, patients with an ejection fraction less than 40% or end-diastolic volume greater than 140 ml/m2 as well as those with end-diastolic dimension greater than 8 cm or end-systolic dimension greater than 5.5 cm have less favorable postoperative survival or further deterioration in ventricular function. Impaired right ventricular function secondary to the increased afterload imposed by pulmonary hypertension generally can be normalized postoperatively. Depression of right ventricular myocardial contractility is not, however, a common pathophysiologic feature in chronic mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Timing of surgical intervention in chronic mitral regurgitation. 369 75


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