Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

It has been generally assumed that most patients with hypertrophic cardiomyopathy (HC) who develop atrial fibrillation (AF) have marked left ventricular (LV) hypertrophy and subaortic obstruction. The morphologic and functional features of this subset of patients with HC have not been systematically investigated. The LV morphology and functional profile of 46 patients with HC and chronic AF were compared with those of 81 control patients with HC and normal sinus rhythm. Contrary to expectations, LV hypertrophy (assessed with 2-dimensional echocardiography) was substantially less marked in the patients with AF than in the control patients, and prevalence of subaortic obstruction was similar in the 2 groups. Maximal LV wall thickness and wall thickness index were lower in patients with AF (18 +/- 2 and 56 +/- 7 mm, respectively) than in control patients (22 +/- 6 and 67 +/- 16 mm, respectively; p less than 0.001). Furthermore, mild LV hypertrophy (maximal LV wall thickness less than or equal to 17 mm confined to 1 ventricular segment) was almost twice as frequent in patients with AF (63%) than in control patients (36%; p less than 0.005). Subaortic obstruction was present in 9 patients with AF (20%) and in 28 control patients (35%; p greater than 0.05). In a subgroup of 22 patients with AF who were followed for 4 to 10 years, 5 patients had marked LV wall thinning (greater than or equal to 5 mm, range 5 to 14). In conclusion, these results demonstrate that most patients with HC and chronic AF have the nonobstructive form of HC, and relatively mild LV hypertrophy.
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PMID:Degree of left ventricular hypertrophy in patients with hypertrophic cardiomyopathy and chronic atrial fibrillation. 153 90

To better understand the pathophysiology of obstruction of left ventricular outflow in hypertrophic cardiomyopathy and to determine the value of intraoperative transesophageal Doppler echocardiography in decision making, 32 consecutive patients undergoing ventriculomyectomy were assessed. The mean preoperative left ventricular outflow gradient was 83 +/- 39 mm Hg and the mean basal septal width was 24 +/- 6 mm. Compared with transesophageal findings in 10 normal control subjects, the mitral leaflets were longer and the coaptation point was abnormal in the patients with obstructive hypertrophic cardiomyopathy (anterior and posterior leaflet lengths in the patients were 31 +/- 4 vs. 22 +/- 3 mm in the control group [p less than 0.00001] and 20 +/- 2 vs. 15 +/- 3 mm in the control group [p less than 0.00001]). The coaptation point in the patient group was in the body of the leaflets at a mean of 9 +/- 2 mm from the anterior leaflet tip, whereas it was at or within 3 mm of the leaflet tip in the normal group. During early systole, the distal third to half of the anterior mitral leaflet angled sharply anteriorly and superiorly (systolic anterior motion), resulting in leaflet-septal contact and incomplete mitral leaflet coaptation in mid-systole. This caused the formation of a funnel, composed of the distal parts of both leaflets, that allowed a jet of posteriorly directed mitral regurgitation to occur in mid- and late systole. The sequence of events in systole was eject/obstruct/leak. Transesophageal echocardiography was also helpful in planning the extent of the resection, assessing the immediate result and excluding important complications. In successful cases, the post-myectomy study showed 1) a dramatic thinning of the septum, with widening of the left ventricular outflow tract to a width similar to that in the normal subjects, 2) resolution of systolic anterior motion and the left ventricular outflow tract color mosaic, and marked reduction or abolition of mitral regurgitation despite persistence of abnormal mitral leaflet length and an abnormal mitral leaflet coaptation point. The routine use of transesophageal echocardiography in patients undergoing surgical myectomy for the treatment of obstructive hypertrophic cardiomyopathy is recommended.
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PMID:Transesophageal Doppler echocardiography in obstructive hypertrophic cardiomyopathy: clarification of pathophysiology and importance in intraoperative decision making. 160 38

We reviewed 201Tl images of a 32 year old man with dilated hypertrophic cardiomyopathy (DHCM). At 22 years of age, when he was diagnosed as having nonobstructive hypertrophic cardiomyopathy (HCM)IVST; 20mm, Dd; 44mm, EF; 62%), 201Tl images showed only a small defect in the anteroseptal segment. At 27 years of age, when he had the first cardiac symptom as palpitation on exertion, his perfusion defect of 201Tl became wider. At 32 years age, he was hospitalized because of deterioration of congestive heart failure. Echocardiography revealed left ventricular wall thinning(IVST; 6mm), left ventricular cavity enlargement (Dd; 63mm) with a large mural thrombus and reduced left ventricular ejection fraction (EF; 32%). Thus 201Tl images may provide useful information on the process of DHCM from HCM.
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PMID:[A case of hypertrophic cardiomyopathy with progressive cavity dilatation--a review of serial 201Tl myocardial imaging]. 192 7

This study describes the long-term outcome of 33 patients with hypertrophic cardiomyopathy who experienced a cardiac arrest but were successfully resuscitated. Cardiac arrest occurred at ages 9 to 62 years (mean 32); five patients survived multiple (two or three) arrests. A variety of treatments were administered; 18 patients with left ventricular outflow tract obstruction underwent ventricular septal myotomy-myectomy or mitral valve replacement and also received drug therapy; 15 patients received medical therapy alone. To date, 22 (67%) of the 33 patients have survived after the initial cardiac arrest for periods of 17 months to 22 years (mean 7 years); 12 patients have survived for greater than or equal to 5 and 6 for greater than or equal to 10 years. Of the 22 survivors, 16 have remained asymptomatic or only mildly symptomatic over the period of follow-up; 6 others have become severely symptomatic with heart failure, including 3 with evidence of left ventricular wall thinning and cavity enlargement. Eight patients ultimately died of natural cardiac causes (suddenly or of progressive heart failure) 7 months to 8.4 years (mean 4 years) after their initial cardiac arrest. Actuarial patient survival was 97 +/- 3%, 74 +/- 9% and 61 +/- 11% after 1, 5 and 10 years, respectively. Event-free rate (defined as actuarial survival without recurrent cardiac arrest of death) was 83 +/- 7%, 65 +/- 9% and 53 +/- 11%, respectively. For this group of patients with hypertrophic cardiomyopathy who were treated in a nonsystematic fashion with a variety of therapeutic strategies, the long-term outcome after surviving a cardiac arrest was variable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term outcome of patients with hypertrophic cardiomyopathy successfully resuscitated after cardiac arrest. 270 10

The influence of long-term treatment with amiodarone on exercise hemodynamics and on left ventricular relaxation was studied prospectively in patients with hypertrophic cardiomyopathy. Rest-exercise hemodynamics (n = 9) and echocardiographic relaxation indexes (isovolumic relaxation time, dPW/dt) (n = 11) were measured in control conditions and after 5 weeks of oral amiodarone treatment (600 mg daily first week, 400 mg daily second week, 200 mg daily afterwards). Long-term amiodarone treatment in patients at rest caused a significant drop in heart rate from 80 +/- 11 to 75 +/- 11 beats/min (p less than .05), a rise in mean pulmonary artery pressure from 19 +/- 7 to 25 +/- 10 mm Hg (p less than .02), and a rise in mean pulmonary capillary wedge pressure from 11 +/- 4 to 17 +/- 8 mm Hg (p less than .05). Systemic arterial pressure, cardiac output, and systemic vascular resistance remained unaltered. Exercise tolerance assessed by serial supine bicycle stress testing was reduced in six of nine patients. Amiodarone treatment caused a significant rise in pulmonary capillary wedge pressure from 22 +/- 8 to 37 +/- 9 mm Hg (p less than .001) at the highest identical workloads and from 26 +/- 10 to 37 +/- 9 (p less than .005) at maximal symptom-limited workloads. Similarly, mean pulmonary artery pressure rose from 37 +/- 15 to 51 +/- 18 mm Hg (p less than .01) at highest identical workloads and from 42 +/- 19 to 51 +/- 18 mm Hg (p less than .01) at maximal symptom-limited workloads. There were no significant differences at maximal exercise level in heart rate, systemic arterial pressure, cardiac output, or exercise factor. Echocardiographic studies performed before and during long-term amiodarone treatment revealed no change in isovolumic relaxation time, end-diastolic or end-systolic posterior wall thickness, and peak posterior wall thinning rate. A negative inotropic action of amiodarone could explain the worsened rest and exercise hemodynamics observed during long-term treatment of patients with hypertrophic cardiomyopathy. Echocardiographic relaxation indexes remained unaltered despite the elevated left ventricular filling pressures. This finding could suggest a deleterious effect of amiodarone on myocardial inactivation, possibly similar in mechanism to the depressed myocardial inactivation observed in hypothyroidism.
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PMID:Effects of long-term treatment with amiodarone on exercise hemodynamics and left ventricular relaxation in patients with hypertrophic cardiomyopathy. 294 32

Ten patients with nonobstructive hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy who had severe symptoms of cardiac failure are described. During a mean follow-up period of 7 years, 6 of these 10 patients showed a substantial increase in left ventricular internal dimension (6 to 15 mm, mean 10) as assessed with M-mode echocardiography, although absolute left ventricular cavity size remained within normal limits in 5 of the 6. Four patients demonstrated substantial septal thinning (5 to 14 mm, mean 8). Left ventricular diastolic function, assessed by radionuclide angiography in nine patients, was impaired in eight who showed decreased peak filling rate (less than 2.5 end-diastolic volumes/s) and prolonged time to peak rate of filling (greater than or equal to 180 ms). Furthermore, left ventricular systolic function, usually supernormal in patients with hypertrophic cardiomyopathy, was depressed (ejection fraction less than or equal to 45%) in six patients. Hence, a subset of patients was identified with nonobstructive hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy who experienced severe cardiac symptoms. The majority of these patients showed both systolic and diastolic left ventricular dysfunction in the presence of a progressive increase in left ventricular internal dimension (but without absolute left ventricular dilation) or ventricular septal thinning or both. Such patients may represent an important component of the natural history of hypertrophic cardiomyopathy which has not been previously fully appreciated.
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PMID:Severe functional limitation in patients with hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy. 294 85

Gated magnetic resonance imaging (MRI) provides excellent anatomic evaluation of the heart, but its capability for assessing cardiac physiology is less clear. Accordingly, regional left ventricular (LV) wall thickening was evaluated by multiphasic transverse images in 37 patients with a variety of myocardial diseases and in 9 normal subjects. Angiography and 2-dimensional echocardiography (2-D echo) were used for comparison. End-diastolic and end-systolic wall thickness, absolute systolic wall thickening and percent systolic wall thickening were determined in 7 regions. Mean systolic wall thickening in normal subjects was not significantly different among the regions. However, there was considerable individual variation in wall thickening, ranging from 18 to 100%. Patients with LV hypertrophy (n = 4), amyloid cardiomyopathy (n = 1), constrictive pericarditis (n = 5), and hypertrophic cardiomyopathy (n = 3) had absolute and percent systolic wall thickening within normal limits. Infarcted segments in patients with ischemic heart disease (n = 17) had reduced absolute and percent systolic wall thickening, often combined with diastolic wall thinning, whereas mean percent systolic wall thickening in adjacent normal myocardial regions was higher than in normal volunteers (p less than 0.001). In patients with coronary artery disease, MRI had a sensitivity and specificity of 93% in detecting regional wall motion abnormalities. Because sagittal images were not acquired, inferior wall motion abnormalities were not assessed by MRI due to parallel wall sectioning in transverse images.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional left ventricular wall thickening by magnetic resonance imaging: evaluation in normal persons and patients with global and regional dysfunction. 294 75

Development or progression of left ventricular hypertrophy has recently been described in children with hypertrophic cardiomyopathy. To determine whether similar changes in magnitude and distribution of left ventricular hypertrophy may also occur in adult patients with this disease, serial assessment of left ventricular wall thickness was obtained with M-mode and two-dimensional echocardiography in 65 patients with hypertrophic cardiomyopathy who were 23 to 50 years of age. The follow-up period was 3 to 6 years (mean 4). None of the 65 patients showed a substantial increase (greater than or equal to 5 mm) in left ventricular wall thickness; however, 9 (14%) demonstrated a substantial decrease (5 to 9 mm). Wall thinning most commonly involved the anterior ventricular septum (seven patients), but was also identified in the posterior septum (six patients), lateral free wall (two patients) and posterior free wall (one patient). In the nine patients with wall thinning, left ventricular end-diastolic diameter increased significantly (from 44 +/- 6 to 51 +/- 6 mm; p less than 0.001); however, in seven of the nine, absolute cavity size remained within normal limits (less than or equal to 52 mm) at the most recent evaluation. Eight of the nine patients with left ventricular wall thinning and relative cavity enlargement were severely symptomatic and one was mildly symptomatic. In conclusion, substantial progression of left ventricular hypertrophy was not identified in any of the study patients. Hence, if such progression occurs in adults with hypertrophic cardiomyopathy, it is probably rare. Conversely, an important minority of adult patients with hypertrophic cardiomyopathy may show progressive left ventricular wall thinning and relative cavity enlargement, which are usually associated with severe cardiac symptoms.
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PMID:Absence of progression of left ventricular hypertrophy in adult patients with hypertrophic cardiomyopathy. 295

We investigated the natural course of 59 patients with hypertrophic cardiomyopathy (HCM) in follow-up periods of one to 13 years and analyzed the clinical, hemodynamic and echocardiographic parameters to determine the factors influencing the prognosis. Among these patients, 44 (75%) remained stable in a compensated condition with or without medications. Five patients died suddenly and two died of congestive heart failure. Heart failure developed in another eight. At the initial evaluation, these 15 patients had high left ventricular end-diastolic pressure (mean: 22 +/- 8 mmHg) significantly higher than that of 44 compensated patients (mean: 13 +/- 6 mmHg, p less than 0.001). There were no differences in age at the initial evaluation between compensated and end stage groups. Atrial fibrillation occurred persistently in three and transiently in two among ten patients with heart failure during follow-up periods. Ventricular dimensions and systolic function did not statistically differ between the two groups. However, six patients with heart failure had cavity dilatation and deteriolated ventricular contractile function at the initial evaluation. Four of them did not show any change in left ventricular hypertrophy, but the regional thinning of the wall was observed in the remaining two. There were no characteristic features to predict sudden death in the clinical, hemodynamic or echocardiographic parameters. Thus, increased left ventricular end-diastolic pressure, atrial fibrillation, left ventricular dilatation and the regional thinning of the left ventricular wall are useful predictive markers for poor prognosis in HCM.
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PMID:[Natural course of hypertrophic cardiomyopathy: clinical, hemodynamic and echocardiographic features in the end stage]. 297 74


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