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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In hypertensive cardiomyopathies, diastolic function is abnormal due to impaired relaxation associated with left ventricular hypertrophy, and a variable degree of reduction in left ventricular compliance may also be present. Abnormal relaxation can be indicated from prolonged isovolumic relaxation time and reduced early diastolic mitral inflow velocity, as well as from a reduced rate of posterior wall thinning and the neg dp/dt estimated from a continuous wave recording of mitral regurgitation. Reduction in left ventricular compliance can be assessed from shortening of the mitral A-wave, and from increased flow reversal in the pulmonary veins at atrial contraction. Non-invasive assessment of LV diastolic function is therefore possible by recording mitral and pulmonary venous flow velocities and posterior LV wall motion.
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PMID:Doppler echocardiographic evaluation of diastolic function in hypertensive cardiomyopathies. 828 71

Coronary aneurysm in Kawasaki's disease (Acute febril infantile mucocutaneous lymph node syndrome, MCLS) may cause sudden death in childhood and ischemic heart disease in adults. We encountered two adult autopsy cases of Kawasaki's disease with multiple coronary aneurysms. The first case was a 56-year-old man who hospitalized due to recurrent syncope since 51 years of age. At age 55 coronary angiography (CAG) had shown multiple aneurysms in the left and right coronary artery. In September 1991, he developed chest pain and was brought to the hospital, almost dead on arrival (DOA). The patient died later the same day despite cardiopulmonary resuscitation. Autopsy findings showed cardiomegaly (470 g) with multiple coronary aneurysms of three coronary arteries. Microscopically, intimal thickening and medial thinning were found in the aneurysmal wall with calcification and disruption of the internal elastic lamina. The second case, a 28-year-old man had been diagnosed with rheumatic fever and mitral regurgitation at 4 years of age. Coronary aneurysms were noted on CAG at 26 years of age. In April 1992, he developed fever and was admitted to a local hospital where he was diagnosed with infectious endocarditis. After his being transferred to our hospital, disturbance of consciousness suddenly developed and he died in September 1992. Autopsy findings showed cardiomegaly (430 g) with left ventricular hypertrophy and multiple coronary aneurysms in left anterior descending coronary artery and left circumflex coronary artery. The aneurysmal wall showed intimal thickening and medial thinning with multiple recanalizations of occlusive lumina and fibrous intimal thickening. The mitral valve showed mild fibrosis and calcification without valvular deformity. There was no evidence of bacterial endocarditis. Both cases were finally diagnosed as Kawasaki's disease. Ischemic heart disease or lesions related to coronary aneurysm in Kawasaki's disease may show an increased incidence in the near future. Kawasaki's disease should have been followed even in adulthood after treatment in childhood.
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PMID:[Adult multiple coronary aneurysms of Kawasaki's disease's sequelae; two autopsy cases]. 952 43

A rare case of aortic and mitral valve aneurysms complicated with infective endocarditis was accurately diagnosed by transesophageal echocardiography. A 57-year-old man with severe aortic regurgitation due to infective endocarditis was admitted to our hospital. Transthoracic echocardiography showed an aortic valve aneurysm on the right coronary cusp and perforations on the other cusps. Transesophageal echocardiography demonstrated a small aneurysm on the anterior leaflet of the mitral valve which was not clearly visualized by transthoracic echocardiography. Color Doppler echocardiography revealed severe aortic regurgitation and mild mitral regurgitation without perforation of the mitral valve aneurysm. Aortic valve replacement and mitral valvuloplasty of the anterior mitral leaflet were performed. The right coronary cusp of the aortic valve showed marked thinning with infiltration of inflammatory cells. The postoperative clinical course was uneventful.
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PMID:[Aortic and mitral valve aneurysms complicated with infective endocarditis: a case report]. 966 5

A 4-month-old girl presented with 2 weeks of symptoms and physical signs of heart failure. Echocardiography demonstrated marked left ventricular dilation, thinning of the myocardium with anterolateral akinesis, mitral regurgitation, a moderate pericardial collection, and an anomalous left coronary artery from the pulmonary artery. At operation there was a tense hemopericardium and a site of imminent rupture through a transmural anterior infarction. The anomalous artery was reimplanted in the ascending aorta, and an extensive infarct resection and ventricular repair performed. Support with a left ventricular assist device was required for 3 days, but the infant subsequently made a satisfactory recovery. Left ventricular rupture is a very rare complication of this lesion, but should be considered if there is evidence of a pericardial collection.
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PMID:Incipient left ventricular rupture complicating anomalous left coronary artery. 1008 69

Valve repair in rheumatic patients poses special problems due to valve deformity and mixed lesions. We present our experience from January 1988 through June 1999, in this retrospective study of 818 patients (377 males). The mean age was 22.8 +/- 11.3 years (range, 2 to 70 years). The cause of mitral regurgitation was rheumatic in 718 (88%) patients, congenital in 51, myxomatous in 34, infective in 7, and ischemic in 8. Most patients (64%) were in New York Heart Association functional class III or IV. Congestive heart failure was present in 116 patients (14%). Reparative procedures included posterior collar annuloplasty (n=710), commissurotomy (n=482), cusp-level chordal shortening (n=237), cusp thinning (n=222), cleft suture (n= 166), and cusp excision/plication (n=42). Operative mortality was 4% (32 patients). Preoperative left ventricular dysfunction, presence of congestive heart failure, and advanced functional class were associated with greater mortality. Follow-up ranged from 1 to 144 months (mean, 44.9 +/- 33.2 months) and was 96% complete. Most survivors (70%) had no or trivial mitral regurgitation. Forty patients required reoperation for valve dysfunction. There were 23 (2.8%) late deaths. Actuarial, reoperation-free, and event-free survival at 11 years were 92.6% +/- 1.0%, 65.0% +/- 10%, and 38% +/- 6.0%, respectively Among the survivors, 85% were in New York Heart Association functional class I. We conclude that mitral valve repair in rheumatic patients, using current techniques, can effectively correct hemodynamic and functional abnormalities with satisfactory results.
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PMID:Mitral valve repair in a predominantly rheumatic population. Long-term results. 1133 Jul 54

The technique and early results of cusp-level chordal shortening for isolated anterior mitral leaflet prolapse in rheumatic mitral regurgitation were presented by us earlier. Here we present our experience from January 1989 through December 2000. Two hundred twenty-six patients underwent this procedure. The mean age was 18 +/- 7.22 years. Preoperatively, 38 (16.8%) patients were in New York Heart Association functional class 11, 160 (70.8%) were in class IIl, and 28 (12.4%) were in class IV. All patients underwent chordal shortening at the cusp level. In addition, 8 patients (3.5%) underwent chordal transfer, and 4 patients (1.8%) received neochordae. Two hundred twenty-one (97.8%) patients underwent posterior annuloplasty using a C-shaped polytetrafluoroethylene collar. In 85 (37.6%) patients, cuspal thinning was also performed. Early mortality was 3.5% (8 patients). Follow-up ranged from 1 to 144 months (mean, 53.02 +/- 31.10 months) and was 94% complete. In 68% of survivors, there was no or trivial mitral regurgitation. Ten patients required reoperation. There were 8 late deaths. Actuarial survival, mitral regurgitation-free survival, and event-free survival were 93.3% +/- 1.7%, 41.8% +/- 8.4%, and 73.6% +/- 6.6%, respectively. Among the 210 survivors, 159 (75.7%) were in New York Heart Association class I, 26 (12.4%) were in class II, 22 (10.5%) were in class III, and 3 (1.4%) were in class IV. We conclude that cusp-level chordal shortening for isolated anterior mitral leaflet prolapse is an effective procedure for correction of anterior mitral leaflet prolapse.
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PMID:Long-term results of cusp-level chordal shortening for anterior mitral leaflet prolapse. 1556 44

A 64-year-old woman was transferred to the intensive care unit with dyspnea and palpitation on effort. Chest x-ray film showed cardiomegaly and pulmonary congestion. We carefully examined for sarcoidosis as a differential diagnosis of heart failure. Serum lysozyme was mildly high, but human atrial natriuretic peptide (HANP) and brain natriuretic peptide (BNP) were strikingly high. Angiotensin converting enzyme was within normal limit. Chest roentgenogram did not reveal bilateral hilar lymphadenopathy. Atrioventricular conduction block was not observed on electrocardiogram. Echocardiographic examination showed left ventricular global hypokinesis with septal thinning and enlargement. Mitral valve regurgitation was recognized by Doppler evaluation. Coronary arteriography showed normal coronary arteries. Endomyocardial biopsy revealed noncaseous epithelioid granulomas containing, Langhans type giant cell accompanied by fibrosis and lymphocyte infiltration. From these data cardiac sarcoidosis was diagnosed. Gallium scintigraphy showed diffuse uptake only in the heart. Treatment with oral prednisolone 20 mg/day was started. Her symptoms improved by several weeks after the medical treatment. In addition, both the value of HANP and BNP were markedly decreased and echocardiogram showed improvement of cardiac systolic function. In Japan, there is a higher incidence of cardiac sarcoidosis than in the West. The prognosis of this condition associated with cardiac dysfunction is reported to be very poor. When progressive heart failure in older patients is seen, cardiac sarcoidosis should also be kept in mind. Endomyocardial biopsy play an important role as the only accurate technique for the diagnosis of cardiac sarcoidosis.
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PMID:[A case of sarcoidosis in which sarocoid granulomas were observed only in the heart]. 1598 67

The chronic elevation in ventricular wall stress secondary to ventricular volume or pressure overload leads to structural remodeling of the muscular, vascular and extracellular matrix components of the myocardium. While initially a compensatory response, the progressive hypertrophy and ventricular dilatation induced by this condition ultimately have a detrimental effect on ventricular function, resulting in heart failure. Fibrillar collagen provides the skeletal framework which interconnects the cardiomyocytes, thereby maintaining ventricular shape and size and contributing to tissue stiffness. Accordingly, these myocardial collagen fibers must be disrupted for ventricular dilatation, sphericalization and wall thinning to occur. The presence of an abundant, latent matrix metalloproteinase (MMP) population which coexists with myocardial fibrillar collagen has been documented. Thus, the potential for collagen degradation to exceed synthesis exists should there be significant activation of this latent MMP system. Mast cells are known to store and release a variety of biologically active mediators including TNF-alpha and proteases such as tryptase and chymase, which can induce MMP activation. Increased cardiac mast cell density has been implicated in the pathophysiology of human end-stage cardiomyopathy and experimental myocardial infarction, hypertension and chronic volume overload secondary to mitral regurgitation and aorto-caval fistula. The potential role of cardiac mast cells in activating MMPs, which then results in fibrillar collagen degradation and adverse myocardial remodeling secondary to chronic volume and pressure overload will be the subject of this review.
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PMID:Cardiac mast cell regulation of matrix metalloproteinase-related ventricular remodeling in chronic pressure or volume overload. 1637 24

We describe herein the case of a 49-year-old female patient with pulmonary sarcoidosis (stage II) with cardiac manifestation. This consisted of systolic dysfunction without dilatation of the left ventricle and severe mitral insufficiency, possibly due to thinning of the posteromedial left ventricular free wall, based on our echocardiographic observations.
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PMID:Echocardiographic evidence of posteromedial hypokinesis of the left ventricle in relation to mitral regurgitation in cardiac sarcoidosis. 1714 15

Although classic Fabry's disease results in multiple causes of death, the cardiac variant of Fabry's disease affects only the cardiac system and results in initial symmetric left ventricular (LV) hypertrophy and later LV dysfunction, asymmetric basal posterior LV wall thinning, restrictive mitral flow, and functional mitral regurgitation with end-stage chronic heart failure (CHF), leading to death. The purpose of this study was to investigate whether these findings predict prognoses in patients with cardiac Fabry's disease. In 13 consecutive men with cardiac Fabry's disease, LV wall thickness, the ejection fraction, mitral E-wave deceleration time, the LV Tei index, and functional mitral regurgitation were measured by echocardiography. Patients were followed for 5 to 96 months (mean 41 +/- 9). Eight patients developed New York Heart Association class III CHF, and 6 experienced cardiac death. A LV Tei index >0.60 and basal posterior LV wall thinning with a ratio of ventricular septal to posterior wall thickness >1.3 significantly preceded CHF and death (Tei index: 4.4 and 5.1 years; posterior wall thinning: 4.0 and 4.7 years), respectively (p <0.05). In conclusion, an increased LV Tei index and asymmetric basal posterior LV wall thinning are important echocardiographic findings that precede CHF and cardiac death in patients with cardiac Fabry's disease.
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PMID:Significance of asymmetric basal posterior wall thinning in patients with cardiac Fabry's disease. 1722 30


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