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)

A total of 4,000 consecutive electrocardiograms covering an 8-yr period was studied and all cases with pure left anterior hemiblock reviewed on the basis of clinical diagnosis and subsequent follow-ups. There were 66 cases in all, representing 1.6% of the total series with an age range of 30--81 and a mean of 53.4 yr; 43 males to 23 females--a ratio of approximately 2 : 1. 34 cases (51.5%) were hypertensives all with a minimum diastolic pressure of 120 mm Hg before treatment. Congestive cardiomyopathy accounted for 16 cases (24.3%) and diabetes mellitus unassociated with other ailments for another 6 cases (9.1%). Other causes included mixed aortic valve disease with 2 cases (3%), endomyocardial fibrosis with 2 cases (3%). In 6 patients (9.1%), all above the age of 70, who had been admitted for minor surgical operations, no cause could be found. This etiological pattern differs from that seen in white populations where ischemic heart disease is by far the commonest cause. The extreme rarity to left anterior hemiblock in rheumatic mitral valve disease is considered of help in separating cases of lone rheumatic regurgitation from those of mitral regurgitation complicating congestive cardiomyopathy if and when diagnostic difficulty arises.
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PMID:Left anterior hemiblock in adult Africans. 64 77

The relation between the apex cardiogram and changes in left ventricular pressure measured by micromanometer, and dimension measured by echocardiography, was studied in 12 normal subjects and 64 patients with heart disease. In 12 patients, the apex cardiogram was delayed with respect to simultaneous left ventricular pressure by 17 +/- 18 ms during the upstroke and 28 +/- 16 ms during the downstroke. In the normal subjects, changes in left ventricular dimension during the upstroke and downstroke of the apex cardiogram were small, amounting to 6 +/- 5 and 21 +/- 7 per cent total excursion, respectively. In 10 patients with mitral regurgitation, there was significant inward wall movement during the upstroke and in 10 patients with aortic regurgitation, significant outward movement during the downstroke, both reflecting valvular regurgitation. In 20 patients with ischaemic heart disease and segmental abnormalities on left ventricular angiography, apex cardiogram-echo dimension relations were abnormal in all, because of inward or outward wall movement during the upstroke, increased outward movement before the 'O' point, or abnormal inward movement during the downstroke. These disturbances were displayed by constructing apex cardiogram-echo dimension loops, which appear to be a sensitive means of detecting incoordinate left ventricular contraction, analogous to those between pressure and dimension.
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PMID:Relation between apex cardiogram and changes in left ventricular pressure and dimension. 83 26

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

The aim of this study was to evaluate the prognosis and functional outcome of mitral regurgitation caused by ischemic papillary muscle dysfunction with respect to treatment, and to determine the role of coronary angioplasty in this context. Thirty patients with severe ischemic mitral regurgitation were followed up for 33 +/- 3 months. Thirteen patients were treated medically (group I) and 17 patients underwent surgery or angioplasty (group II). The 3-year survival was 59.5% (45.6% in group I and 70.2% in group II). Angioplasty was only used in paroxysmal mitral regurgitation caused by papillary muscle ischemia. This technique resulted in spectacular immediate results in three patients with pulmonary edema caused by mitral regurgitation during myocardial ischemia. Surgical correction of mitral regurgitation should be considered without delay if angioplasty is not feasible or if the regurgitation is permanent or severe. Widening the indications of surgery or angioplasty should result in an improvement of the prognosis of these high-risk patients.
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PMID:Treatment of severe mitral regurgitation caused by ischemic papillary muscle dysfunction: indications for coronary angioplasty. 154 93

Ten healthy (aged 28 to 39) and ten heart failure NYHA II (aged 19 to 49) male subjects were prospectively studied under no drugs, under furosemide (40 mg/day), under captopril (150 mg/day) and under their association. Arterial compliance (ml/mmHg) was measured in all subjects at rest and supine. Heart failure etiology was dilated cardiomyopathy or ischemic heart disease without significant regurgitation. Arterial compliance was significantly higher in healthy than in heart failure patients in all studied conditions (p less than 0.001) (healthy = 2.2 + 0.29 vs. heart failure = 0.79 + 0.14). Neither single drug nor their association induced any change in healthy subjects. Arterial compliance progressively increased in heart failure with furosemide, captopril, and their association (no drug = 0.79 + 0.14; furosemide = 0.87 + 0.15; captopril = 0.94 + 0.15 and furosemide + captopril = 0.99 + 0.14). Captopril induced a higher increment than furosemide (p less than 0.001) and their association even a higher increment (p less than 0.001) than any single drug. Thus captopril and/or furosemide increased arterial compliance in heart failure but not in healthy subjects, possibly through changes in arterial wall edema and smooth muscle contraction.
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PMID:Effect of drugs on a noninvasive index of arterial compliance in healthy and heart failure patients. 174 91

A 24-year-old male presented with exertional dyspnoea of one year's duration. Echocardiography revealed an unruptured aneurysm of the left sinus of Valsalva distorting the mitral valvar apparatus and producing severe regurgitation in the absence of myocardial ischemia or infarction. We propose an alternate mechanism for the mitral regurgitation.
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PMID:Aneurysm of the left sinus of Valsalva causing severe mitral regurgitation. 186 35

To determine the sequelae of transient myocardial ischemia (TMI) in term infants, we reviewed clinical and investigative data in 59 infants (37 male, 22 female) with structurally normal hearts admitted over the 2-year period of 1983-1985. Twenty-three were diagnosed prior to admission as cases of birth asphyxia (5-min Apgar score less than 6), and 36 had signs of persistent fetal circulation with electrocardiographic (ECG) changes of ischemia greater than 24 h after birth. Murmurs of atrioventricular valve regurgitation (AVVR), detected in 28 patients, were confirmed in 23 of the 24 patients investigated. The murmurs resolved over a 2-day to 6-month period (median 6 days). In three patients, AVVR, left ventricular dyskinesia, and ECG anomalies persisted for 2 months (until death), 4 months, and 48 months. Initial ECGs were abnormal in 57 patients, and (of those reviewed) 60% returned to normal over a 6-day to 7-month period (median 2 months). Residual ECG anomalies included second-degree AV block and persistent ST-T wave changes. Ten patients died from noncardiac causes. Neither the presence nor resolution of AVVR correlated significantly with the severity of birth asphyxia using the Apgar score, nor with the severity of the ischemic changes on the ECG. Although the cardiovascular sequelae of myocardial ischemia are usually transient, the data should prompt the need for careful review after the initial admission.
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PMID:Persistence of atrioventricular valve regurgitation and electrocardiographic abnormalities following transient myocardial ischemia of the newborn. 259 71

The purpose of this retrospective study was to consider impaired renal function in patients with severe congestive heart failure after converting enzyme inhibition and to emphasize the characteristics of this population. The study concerned 26 patients (pts), 72.5 +/- 8.1 years old, with a severe congestive heart failure (NYHA Class IV). Before treatment serum creatinine was slightly increased and the introduction of angiotensin converting enzyme inhibitor (ACEI) - Captopril 58.9 +/- 17.3 mg/j or enalapril 9.2 +/- 4.4 mg - impaired renal function from 132.0 +/- 50.7 mumol/l to 183.5 +/- 139.3 mumol/l (n = 26; p less than 0.05). Patients were separated in 3 groups: in group I; 15 pts, serum creatinine remained unchanged under ACEI in despite of the significant decrease of blood pressure (BP); from 140.7 +/- 24.0/82.5 +/- 13.4 to 120.3 +/- 12.8/71.8 +/- 8.7 mmHg (p less than 0.01). The cause of heart failure was an ischemic heart disease (IHD) in 15 patients (chi 2 test, p less than 0.05), a dilated cardiomyopathy in 4 pts and an aortic or mitral valvular regurgitation in 2 pts. In contrast renal function was significantly impaired in group II; serum creatinine increased from 120.8 +/- 25.2 to 189.0 +/- 80.7 mumol/l under ACEI. BP remained unchanged 136.9 +/- 29.0/78.1 +/- 4.9 and 118.7 +/- 13.6/75.6 +/- 7.6 mmHg respectively before and after treatment. There was 4 pts with dilated cardiomyopathy, 4 pts with mitral or aortic valvular regurgitation and only one with IHD. The introduction of an ACEI in two pts--group III--with severe tricuspid regurgitation induced an acute and reversal renal failure (serum creatinine at 600 mumol/l).
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PMID:[Renal insufficiency and treatment of persistent cardiac insufficiency with converting enzyme inhibitor]. 273 17

The syndrome of primary mitral leaflet billow, with or without prolapse, is associated with myxomatous degeneration of the mitral valve apparatus, mainly the posterior leaflet, and the syndrome may be familial. It manifests clinically with an isolated nonejection systolic click (billow), a murmur of mitral regurgitation that is usually late systolic (prolapse), or a combination of murmur and click. Echocardiography identifies and assesses the extent of the billowing of mitral leaflet bodies but there are no specific echocardiographic criteria that can differentiate normal from pathological billowing. Similarly, a prolapsed leaflet is not detected echocardiographically when there is localized and mild failure of leaflet edge apposition but a more severely prolapsed, or flail, leaflet can be demonstrated and confirmed by that technique. Symptoms of the syndrome include anxiety, chest pain and palpitations. The resting electrocardiogram may show ST segment and T wave abnormalities. The majority of patients have a benign course and require reassurance only. Complications include systemic emboli, infective endocarditis, progression to severe mitral regurgitation, arrhythmias and, rarely, sudden death. Patients with prolapse of a leaflet edge are more likely to develop complications than those with only billowing of the leaflet bodies. Surgery, preferably valvuloplasty, is required for severe regurgitation and may also be indicated for potentially lethal tachyarrhythmias unresponsive to medical therapy. Mitral leaflet billow and prolapse may be secondary to, or associated with, many conditions. The prognosis is then principally that of the underlying disease of which ischemic heart disease and hypertrophic cardiomyopathy are the most important.
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PMID:Mitral valve billowing and prolapse: perspective at 25 years. 304 85

The aim of this study was to assess the diagnostic value of pulsed and continuous wave Doppler in mitral regurgitation. One hundred and twenty-one patients (64 women and 57 men aged 13 to 76 years, average 54 years) investigated for mitral regurgitation or ischaemic heart disease underwent left ventricular angiography and continuous wave and pulsed Doppler echocardiography. In addition to clinical examination, they also underwent M mode, 2D echocardiography and phonocardiography. They were divided into two groups according to the presence or absence of mitral regurgitation on angiography, chosen as the reference method. Group I comprised 51 patients with angiographic regurgitation, and Group II 70 patients without mitral regurgitation. The sensitivity of the Doppler examination was 98%. Of the 51 patients in Group I there was only one false negative in a patient with doubtful angiographic regurgitation in the context of an endocardial cushion defect. In comparison, the sensitivity of clinical examination and phonocardiography were 74.5% and 80% respectively; 13 cases of mitral regurgitation on angiography and Doppler echocardiography had no auscultatory signs. The specificity of the Doppler examination was 92.8%; 5 of the 70 patients in Group II had unquestionable systolic turbulence in the left atrium and 2D echocardiography showed the possible mechanism of these valvular leaks in 3 cases: 1 bivalvular prolapse, 1 rheumatic valvular thickening and 1 papillary muscle dysfunction. We interpret these 5 cases as being true mitral regurgitation but intermittent or too slight to be visible on angiography. The positive predictive value of systolic turbulence in the left was 90.9% and the negative predictive value was 98.4%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pulsed and continuous Doppler in qualitative and quantitative diagnosis of mitral insufficiency]. 309 Sep 65


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