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

A retrospective study of Chagas's heart disease was carried out by a review of necropsy reports with special reference to the lesion known as the apical aneurysm. It was concluded that this lesion was more frequent in men, was unrelated to age, and was unrelated to heart weight. Patients dying of the cardiac consequences of Chagas's cardiomyopathy were more likely to have an apical aneurysm than those whose death was unrelated to the disease but the mode of death (sudden, or with heart failure) was unconnected with its presence. Transillumination from within the ventricle at necropsy was not only useful in demonstrating the aneurysm but also showed areas of myocardial thinning elsewhere. Thrombosis within the lesion was frequent. The aetiology of the apical aneurysm is discussed and it is concluded that while ischaemia, inflammation, thrombosis, and mechanical factors may produce and localise this lesion, the underlying cause is the basic pathogenetic process-parasympathetic nerve cell destruction.
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PMID:Apical aneurysm of Chagas's heart disease. 729 39

End stage heart failure due to ischemic (ICM) or dilated (DCM) cardiomyopathy is characterized by a dilated, relatively thin-walled ventricle. The hypothesis has been proposed that the structural basis of ventricular expansion is due to side-to-side slippage of myocytes within the wall. Although this represents one potential mechanism for the observed phenomena of chamber dilatation and subsequent wall thinning, the degree of slippage claimed is not necessarily in harmony with the magnitude of chamber enlargement and mural thinning. Moreover, sarcomere extension was not examined in the base to the apical regions of the heart, leaving open the question as to the role of changes in resting sarcomere length in acute chamber dilatation. In this regard, an alternative etiology for the detrimental cardiac architectural rearrangement seen in dilated failure can be supplied by postulating the occurrence of maladaptive remodeling of cardiac myocyte morphology. In this model, myocytes increase in length by an increase in the number of sarcomeres in series, thus increasing chamber diameter in an attempt to maintain cardiac output. However, these cells do not enlarge to any significant degree in the transverse diameter preventing the heart from developing adequate force. This hypothesis is supported by recent evidence from patients with ICM and DCM indicating that myocyte lengthening alone could account for all the dilatation observed. Furthermore, it appears that the thinning of the ventricular wall in failure is due to inadequate transverse growth of cardiac myocytes coupled with scattered myocyte cell loss throughout the ventricular wall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Structural remodeling and mechanical dysfunction of cardiac myocytes in heart failure. 760 3

Clinical and electrocardiographic features of 227 patients who died of an acute myocardial infarction (AMI) were compared with those of 150 survivors of a first AMI. Left ventricular (LV) free wall rupture was found in 93 patients aged > 50 years, but not in 134. The incidence of healed infarct (4 [4%] vs 50 [37%], p < 0.001), heart failure (11 [12%] vs 112 [84%], p < 0.001), and bundle branch block (11 [12%] vs 54 [40%], p < 0.001) was lower in patients with than without LV rupture. In patients with anterior AMI and early rupture (1 day), admission ST elevation was higher than in those with late LV rupture (> 1 day, 6.8 +/- 4.0 vs 4.0 +/- 2.7 mm, p < 0.01). However, lateral wall AMI had minimal ST elevation and accounted for 10% of ruptures. On day 2, the decrease in ST segment in patients with late LV rupture was less than in survivors (0.5 +/- 1.6 vs 3.2 +/- 2.9 mm, p < 0.001). Admission systolic blood pressure in patients who had early rupture was higher than in survivors (155 +/- 22 vs 137 +/- 22 mm Hg, p < 0.001) and in those with late rupture (135 +/- 23 mm Hg, p < 0.001). Late rupture was associated with infarct thinning and triggered by a physical strain in 18 of 45 patients (40%); infarct thinning, however, was present only in 4 of 48 patients (8%) with early rupture (p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relevance of electrocardiographic findings, heart failure, and infarct site in assessing risk and timing of left ventricular free wall rupture during acute myocardial infarction. 767 73

The interactions of the systemic and myocardial adaptations during and after rapid ventricular pacing, a model of heart failure, were assessed in conscious, unstressed dogs. Ultrasonic probes and vascular catheters were surgically implanted into dogs for measurements of blood flows and pressures during 3 weeks of pacing and after 2 months of recovery. Three weeks of tachycardia (260 beats/min) resulted in a marked reduction in hemodynamic parameters and left ventricular dilatation, with caudal wall thinning throughout the pacing period and 1 week of recovery. Sinus rhythm resumed after the pacer was turned off, with return toward normal in hemodynamic parameters; however, left ventricular dilatation and ventricular remodeling, with significant fibrosis, loss of myocytes, and hypertrophy of the surviving cells were still present after 2 months of recovery. In conclusion, even though hemodynamic parameters normalized during recovery, adaptive myocardial remodeling caused permanent ventricular fibrosis, hypertrophy, and increased cardiac filling pressures.
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PMID:Myocardial effects of repetitive episodes of rapid ventricular pacing in conscious dogs: surgical creation, echocardiographic evaluation, and morphometric analysis. 784 53

To analyze the clinical features of cardiac sarcoidosis, we reviewed case reports and clinical investigations from Japan and other countries. Female patients were more frequently affected in this disease in Japan. Cardiac sarcoidosis is characterized by a high incidence of complete atrioventricular block, right bundle branch block, and ventricular arrhythmias on the electrocardiogram. Echocardiography often reveals left ventricular dilatation with systolic dysfunction and wall thickening or thinning. Radionuclide testings, such as, thallium-201, gallium-67 or technetium-99m pyrophosphate, are useful for detecting cardiac involvement and evaluating efficacy of corticosteroid therapy in patients with sarcoidosis. Most of the patients died due to recurrent or refractory heart failure. It is noteworthy that cases of sudden death during stable cardiac function have become infrequent.
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PMID:[Cardiac sarcoidosis]. 804 45

Turkey poults fed furazolidone (Fz) in high concentrations (700 ppm) develop dilated cardiomyopathy (Fz-DCM). We tested whether five cardioactive agents were cardioprotective in this model of heart failure, ie, whether they prevented dilatation and wall thinning and improved contractile performance. We compared the effects of chronic administration of a beta 1-selective and a nonselective beta-receptor antagonist, an alpha-receptor antagonist, and two Ca2+ channel antagonists in the presence of Fz administration. The greatest cardioprotection was found with treatment with either propranolol or nifedipine. At the gross morphological level, the effect of propranolol (a nonselective beta-adrenergic antagonist) was greater than the effect of atenolol (a selective beta 1-adrenergic antagonist), and the effect of nifedipine was greater than that of verapamil (Ca2+ channel antagonists), with all agents more cardioprotective than phenoxybenzamine (an alpha 1-adrenergic > alpha 2-adrenergic antagonist). Differences in cardioprotective efficacy of each agent increased with increased concentration. These data indicate that the dose and choice of a specific type of Ca2+ channel antagonist or beta-receptor antagonist might be important in the treatment of dilated cardiomyopathy. All agents that were cardioprotective caused similar functional improvements at both the whole heart and isolated muscle levels. Compared with control animals, Fz-DCM animals showed a significant reduction in peak left ventricular (LV) developed pressure (92 +/- 17 versus 143 +/- 24 mm Hg, P < .05), +dP/dt (1151 +/- 219 versus 2454 +/- 549 mm Hg/s), and -dP/dt (1128 +/- 291 versus 1875 +/- 396 mm Hg/s), with a significant increase in LV end-diastolic volumes (2.8 +/- 0.7 versus 0.16 +/- 0.1 mL for control animals, P < .05). In contradistinction, LV + dP/dt and -dP/dt values for animals receiving Fz plus a cardioactive agent that demonstrated cardioprotection were not significantly different from control values. Peak LV developed pressures were also similar for Fz animals receiving an agent that demonstrated cardioprotection and control animals not receiving any pharmacologic agent. Isolated muscles from Fz-DCM animals as well as animals receiving Fz plus cardioprotective pharmacologic agents responded normally with regard to increasing extracellular Ca2+ concentrations. Peak twitch forces were greater for animals receiving cardioprotective agents plus Fz than control animals not receiving any pharmacologic agents or Fz alone. At higher stimulation rates, Fz-DCM muscles demonstrated a significantly reduced peak twitch force (4 +/- 0.5 versus 1.5 +/- 0.4 g/mm2 for control muscles versus Fz-DCM muscles, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Differences in cardioprotective efficacy of adrenergic receptor antagonists and Ca2+ channel antagonists in an animal model of dilated cardiomyopathy. Effects on gross morphology, global cardiac function, and twitch force. 822 79

Arterial hypertension leads to left ventricular hypertrophy. In proportion to increased left ventricular systolic pressure, left ventricular hypertrophy is considered to be of adaptive nature from the point of view of wall stress regulation. In the beginning, left ventricular function is normal, whereas diastolic filling is already compromised by the process of hypertrophy and altered ventricular geometry. In case of ventricular dilation and wall thinning, wall stress increases and leads to an increment in myocardial oxygen demand and a decrease of left ventricular ejection fraction. This is followed by a further decline in intrinsic myocardial contractility and a decrease in the elastic material properties of the myocardium. The structure of the myocardium is characterized by myocyte hypertrophy, a process of reactive and reparative fibrosis and alterations of the coronary microcirculation. Coronary vasodilator reserve is markedly impaired and is likely to initiate a process of malperfusion and malnutrition under increased metabolic demands. Particularly, the combined involvement of myocytes, interstitium, and intramyocardial vasculature appears to predispose to late heart failure after prolonged exposure to chronic pressure overload in arterial hypertension.
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PMID:Heart failure on the basis of hypertension. 848 35

Rupture of the left-ventricular free wall may not always result in immediate irreversible hemodynamic collapse. We report a series of five patients (4 male, 1 female; age 59-79 years) successfully operated for postinfarction free-wall rupture with good long-term results. Two patients presented with syncopy and acute tamponade three days after an acute myocardial infarction. In two patients with atypical chest pain and congestive heart failure, a large pericardial effusion and an extreme localized thinning of a myocardial scar region was seen several weeks after an uncomplicated myocardial infarct. In one patient a pseudoaneurysm was detected, which developed asymptomatically within three weeks after a posterior myocardial infarct. In all cases myocardial rupture was suspected after an echocardiographic examination. At surgery a hemopericardium and a localized rupture site were found. The surgical procedure included closure of the defect by direct suture or patch, CABG in 3 cases, and mitral valve replacement in one patient. The postoperative course was uneventful, only one patient needed IABP for 24 hours. Three patients returned to NYHA functional class I, one patient to class II, and one patient to class III. The latter patient died of heart failure 17 months postoperatively, and the other patients are still alive 4,18,24, and 26 months postoperatively. Thus clinical representation of left-ventricular free-wall rupture after myocardial infarction can be highly variable. But close cooperation between experienced echocardiographers and surgeons may allow successful corrections with good long term-results.
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PMID:Clinical presentation of rupture of the left-ventricular free wall after myocardial infarction: report of five cases with successful surgical repair. 878 31

Left ventricular hypertrophy is an adaptive response to long standing hypertension. However, the influence of left ventricular hypertrophy with hypertension on extent of infarct expansion has not been studied. We compared the effects of left ventricular hypertrophy with hypertension on infarct expansion in spontaneously hypertensive rats (SHR, n = 76), Wistar-Kyoto rats (WKY; n = 46) and spontaneously hypertensive rats treated with delapril, an angiotensin converting enzyme (ACE) inhibitor (SHRD; n = 39). The survival rates at 7 days after myocardial infarction were 41%, 24%, and 46% for WKY, SHR, and SHRD. The survival rate of SHR was significantly lower than those of both SHRD and WKY (P < .05). In the surviving rats (18 SHR, 19 WKY, 18 SHRD), both left ventricular cavity area (LCVA) and the infarct segment length per the noninfarct segment length (FW/IVS), measured as indices of left ventricular dilation, were significantly less in SHR and SHRD than in WKY, and the thickness of the left ventricular free wall (Wth), used as an index of left ventricular thinning, was significantly higher in both SHR and SHRD than in WKY (P < .01). However, there was no significant difference in FW/IVS, LCVA, and Wth between SHR and SHRD. Hemodynamic findings 1 week after coronary occlusion demonstrated that all rats were in heart failure, and there were no significant differences in hemodynamics among the three groups. In conclusion, our findings showed that hypertrophy with hypertension reduced infarct expansion, but that reduction of blood pressure by ACE inhibitor did not reduce infarct expansion more than hypertrophy did. However, this finding suggest that an ACE inhibitor may improve the rate of survival of patients with left ventricular hypertrophy with hypertension.
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PMID:Effects of chronic hypertension and left ventricular hypertrophy on the extent of infarct expansion in rats. 886 21

Progressive changes typically occur in left ventricular (LV) architecture following moderate- to large-sized myocardial infarction (MI). These changes include early expansion and thinning of the infarct zone and subsequent increase in myocardial mass within the non-infarcted zone, with LV dilatation and loss of the normal elliptical configuration of the LV cavity. These changes are accompanied by impaired myocyte function and advancing clinical expression of heart failure. Numerous animal and human studies have documented inhibition of LV remodeling post-MI by angiotensin converting enzyme (ACE) inhibitors. Although the ideal timing for initiating treatment remains uncertain, evidence exists that benefit persists long after the time of initial injury. Mechanisms for the effects of ACE inhibitors on LV remodelling may be dependent on changes in myocardial load, may be load independent, or both. These effects are likely to be mediated by reductions in circulating and local tissue concentrations of angiotensin II and in bradykinin degradation. Regardless of the exact mechanism or mechanisms by which ACE inhibitors exert their favourable influence on LV remodelling, it is likely that this effect is a key mediator of the documented clinical benefits afforded by treatment with this class of agents.
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PMID:Role of angiotensin converting enzyme inhibitors in preventing left ventricular remodelling following myocardial infarction. 886 35


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