Endomyocardial biopsy pathology in insulin‐dependent diabetic patients with abnormal ventricular function

Sutherland, Carolyn; Fisher, B. M.; Frier, Brian M.; Dargie, Henry J.; More, I. A. R.; Lindop, G. B. M.

doi:10.1111/j.1365-2559.1989.tb02200.x

Cited by 58 publications

(23 citation statements)

References 20 publications

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“…The traditional techniques for assessment of myocardial blood flow have been either invasive (24) or based on the administration of ionizing agents (6) and do not readily allow repeated measurements of dynamic changes. However, myocardial blood flow is modulated in keeping with metabolic demands also in diabetes with its functional and structural modifications of the myocardium (25,26). Changes in myocardial blood flow are mainly mediated by alterations in flow velocity at the level of subepicardial coronary arteries but less so at the level of the microcir-culation because coronary autoregulation stabilizes perfusion pressure, which controls flow velocity (27).…”

Section: Discussionmentioning

confidence: 99%

C-Peptide Exerts Beneficial Effects on Myocardial Blood Flow and Function in Patients With Type 1 Diabetes

et al. 2002

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Myocardial dysfunction, perfusion abnormalities, and the extent to which these abnormalities may be reversed by C-peptide administration was assessed in type 1 diabetic patients. Eight patients were studied before and during a 0.84-mg/kg dipyridamole administration using a randomized double-blind crossover protocol with infusion of C-peptide (6 pmol ⅐ kg -1 ⅐ min -1 ) or saline during 60 min on two different days. Myocardial function was measured as peak myocardial velocity during systole (Vs) and early diastole (Vd) by pulsed tissue Doppler imaging. Myocardial contrast echocardiography was used for assessment of myocardial blood volume (SI max ) and myocardial blood flow index (MBFI) calculated from the relation between trigger interval and signal intensity. Eight age-matched healthy volunteers served as control subjects. In the basal state, Vd (13.8 ؎ 0.6 vs. 15.6 ؎ 0.5 cm/s, P < 0.04) and SI max (6.6 ؎ 0.6 vs. 8.2 ؎ 0.6 a.u. P < 0.04) were reduced in patients compared with control subjects. Dipyridamole administration significantly increased indexes of myocardial function and blood flow to a similar extent in patients and control subjects. During C-peptide administration, Vs and Vd increased by 12% (P ‫؍‬ 0.03), SI max increased from 6.6 ؎ 0.6 to 8.1 ؎ 0.7 a.u. (P < 0.02), and MBFI increased from 3.3 ؎ 0.4 to 5.3 ؎ 0.9 (P < 0.05). The results demonstrate that type 1 diabetic patients have impaired myocardial function and perfusion in the basal state that can be improved by short-term replacement of C-peptide. Diabetes 51:3077-3082, 2002

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Section: Discussionmentioning

confidence: 99%

C-Peptide Exerts Beneficial Effects on Myocardial Blood Flow and Function in Patients With Type 1 Diabetes

et al. 2002

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“…Diabetes is responsible for specific vascular changes, cardiac autonomic neuropathy and specific structural changes, mainly fibrosis and microangiopathy (Sutherland et al, 1989). Obesity-associated cardiomyopathy is mainly caused by an excess in blood volume.…”

Section: Susceptibility Factorsmentioning

confidence: 99%

Phenotypic plasticity of adult myocardium: molecular mechanisms

Swynghedauw

2006

Journal of Experimental Biology

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Molecular cardiologists, even clinical cardiologists, are familiar with phenotypic plasticity. They call it remodelling*. Myocardial and vascular remodelling have primarily a mechanical origin and an adaptive significance. Cardiac remodelling (CR) occurs in response to chronic mechanical overloading, and arterial remodelling is a response to permanent arterial hypertension (Lompré et al., 1979;Swynghedauw, 1999;Levy and Tedgui, 1999). CR leads to heart failure and, with cancer, is one of the major causes of death in our countries, so cardiac plasticity is a major public health problem. This review will only focus on myocardial remodelling (excluding the remodelling of coronary vessels).This review will start from the most common clinical conditions † , namely CR occurring after myocardial infarction or chronic essential arterial hypertension, and will consider Cardiac phenotypic plasticity (so-called cardiac remodelling, CR) is characterized by changes in myocardial structure that happen in response to either mechanical overload or a loss of substance such as that occurring after myocardial infarction.Mechanosensation is a widespread biological process and is inextricably mixed with other transduction systems from hormones and vasopeptides, which ultimately produce post-translational modifications of transcription factors. The expression of the four main transcription factors during cardiogenesis is also enhanced as a link to foetal reprogramming.CR results from re-expression of the foetal programme, which is mostly adaptive, but also from several other phenotypic modifications that are not usually adaptive, such as fibrosis. (i) The initial determinant is mechanical, and reexpression of the foetal programme includes a global increase in genetic expression with cardiac hypertrophy, reexpression of genes that are normally not expressed in the adult ventricles, repression of genes not expressed during the foetal life, and activation of pre-exisiting stem cells. Microarray technology has revealed a coordinated change in expression of genes pertaining to signal transduction, metabolic function, structure and motility, and cell organism defence. The physiological consequence is a better adapted muscle. (ii) During clinical conditions, the effects of mechanics are modified by several interfering determinants that modify CR, including senescence, obesity, diabetes, ischemia and the neurohormonal reaction. Each of these factors can alter myocardial gene expression and modify molecular remodelling of mechanical origin.Finally, as compared to evolutionary phenotypic plasticity described in plants and insects in response to variations in environmental conditions, in CR, the environmental factor is internal, plasticity is primarily adaptive, and it involves coordinated changes in over 1400 genes. Study of reaction norms showed that the genotypes from different animal species are similarly plastic, but there are transgenic models in which adaptation to mechanics is not caused by hypertrophy but by qualitative changes in gene...

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“…There are several possible mechanisms that explains the association of diabetes mellitus with lack of microvascular reperfusion following revascularization. Several clinical studies have demonstrated that maximal coronary vasodilation was impaired in diabetic patients (18,19), possibly in part because of microvascular structural abnormalities in coronary resistance vessels including arteriolar thickening, perivascular accumulations of connective tissue and capillary microaneurysms (20,21). Endotheliumdependent vascular relaxation has also been reported to be impaired in diabetic patients (22,23).…”

Section: Proposed Mechanisms Of Microvascular Reperfusion Injury In Dmentioning

confidence: 99%

Diabetes Mellitus is Associated with Insufficient Microvascular Reperfusion following Revascularization for Anterior Acute Myocardial Infarction

et al. 2003

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Objective The purpose of this study was to test the hypothesis that lack of microvascular reperfusion following revascularization might be associated with a poor clinical outcome in diabetic patients with acute myocardial infarction (AMI).Methods Westudied 134 patients with a first anterior AMI whounderwent successful revascularization within 6 hours. Weassessed microvascular reperfusion by using electrocardiogram recordings just before revascularization and on return to the coronary care unit. Lack of microvascular reperfusion was defined as the absence of decrease of >20%in the sum of ST segment elevation (EST).Results Twenty-four patients had diabetes and 110 patients did not. EST before revascularization was similar between diabetic and nondiabetic patients. After revascularization, reduction of UST was significantly smaller (1.3±8.4 mm vs 6.5±10.8 mm, p=0.03), and lack of microvascular reperfusion was significantly more frequent (62.5% vs 33.6%, p=0.01) in diabetic patients. A multivariate analysis showedthat diabetes was associated with insufficient microvascular reperfusion (odds ratio 3.18, p=0.03).Major adverse cardiac events occurred more frequently in patients with a lack of microvascular reperfusion (30.8% vs 15.9%, p=0.04). Conclusion These findings suggest that lack of microvascular reperfusion following revascularization may be one of the mechanisms of a poor clinical outcome in diabetic patients with AMI. (Internal Medicine 42: 554-559, 2003)

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Endomyocardial biopsy pathology in insulin‐dependent diabetic patients with abnormal ventricular function

Cited by 58 publications

References 20 publications

C-Peptide Exerts Beneficial Effects on Myocardial Blood Flow and Function in Patients With Type 1 Diabetes

C-Peptide Exerts Beneficial Effects on Myocardial Blood Flow and Function in Patients With Type 1 Diabetes

Phenotypic plasticity of adult myocardium: molecular mechanisms

Diabetes Mellitus is Associated with Insufficient Microvascular Reperfusion following Revascularization for Anterior Acute Myocardial Infarction

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