Diastolic dysfunction and abnormalities of the microcirculation in type 2 diabetes

Brooks, Belinda; Franjic, B.; Ban, Camelia R; Swaraj, Kiran; Yue, Dennis K.; Celermajer, David S.; Twigg, Stephen M.

doi:10.1111/j.1463-1326.2007.00803.x

Cited by 64 publications

(41 citation statements)

References 45 publications

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“…Previous studies demonstrated the association between hsCRP and microvascular complications, including nephropathy and retinopathy, in patients with hypertension (Shantha et al 2010) and diabetes (Kang et al 2004;Kajitani et al 2010). Because LV diastolic dysfunction is also produced by microvascular complication in hypertension (Hoenig et al 2008) and diabetes (Brooks et al 2008), LV diastolic dysfunction is likely to be associated with increased hsCRP.…”

Section: Discussionmentioning

confidence: 99%

Association between High-Sensitivity C-Reactive Protein and Left Ventricular Diastolic Function Assessed by Echocardiography in Patients with Cardiovascular Risk Factors

Masugata

Senda

Inukai

et al. 2011

Tohoku J. Exp. Med.

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High-sensitivity C-reactive protein (hsCRP) has been demonstrated to play a causal role in atherosclerosis and to predict cardiovascular events in the general population. On the other hand, left ventricular (LV) hypertrophy and diastolic dysfunction assessed by echocardiography can also predict cardiovascular events in patients with cardiovascular risk factors. However, there are few data regarding the relationships among hsCRP, LV hypertrophy, and diastolic function. We examined the relationships among hsCRP, LV hypertrophy, and diastolic function in 185 patients (65 ± 11 years), who had no overt heart disease, but had cardiovascular risk factors, including hypertension, diabetes, and dyslipidemia. Echocardiography was performed to measure the left ventricular mass index (LVMI) as a parameter of LV hypertrophy. LV diastolic function was assessed by the ratio (E/A) of early (E) and late (A) diastolic transmitral flows, early diastolic mitral annular velocity (E´), and the ratio (E/E´) of E to E´using Doppler echocardiography. The hsCRP was correlated with LVMI (r = 0.228, p = 0.002), E´ (r = −0.276, p < 0.001), and E/E´ (r = 0.419, p < 0.001). The E/E´ as a parameter of LV diastolic function showed the closest correlation to hsCRP. These results indicate that elevated hsCRP reflects LV diastolic dysfunction rather than LV hypertrophy. We therefore suggest that hsCRP may be a marker of subclinical LV diastolic dysfunction in patients with cardiovascular risk factors.

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Section: Discussionmentioning

confidence: 99%

Association between High-Sensitivity C-Reactive Protein and Left Ventricular Diastolic Function Assessed by Echocardiography in Patients with Cardiovascular Risk Factors

Masugata

Senda

Inukai

et al. 2011

Tohoku J. Exp. Med.

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“…2,12 Not only the famous phenomenon of "silent myocardial ischemia" in diabetic patients suffering coronary artery disease, 13 but diabetic cardiac remodeling also progresses asymptomatically but significantly enough to elevate the high-sensitivity troponin-T level. 14 Microvasculopathy is a primary feature of diabetic myocardial remodeling, 2, 15,16 but no surrogate could directly monitor the disease progression. Furthermore, the term DMC is a matter of debate because DMC has been originally specified only for HF-REF patients, although the current diagnostic criteria for DMC include HF-PEF.…”

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confidence: 99%

Diabetes-Related Heart Failure

Bando

Murohara

2014

Circ J

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As the link between heart failure (HF) and diabetes mellitus (DM) becomes unignorable, so the need is further increasing for pathological comprehension: What is "diabetic cardiomyopathy (DMC)?" In response to current concern, the most updated guidelines stated by the ACCF/AHA and by the ESC/EASD take one step further, including the definition of DMC, although it is a matter yet to be completed. For more than 40 years, coronary artery disease and hypertension have been considered as the main causes of diabetes-related cardiac dysfunction. HF was originally considered as a result of reduced left ventricular ejection fraction (HF-REF); however, it has been recognized that HF symptoms are often observed in patients with preserved EF (HF-PEF). DMC includes HF with both reduced and preserved entities independent of coronary stenosis and hypertension. Cardiologists are thus facing a sort of chaos without clear guidelines for the "deadly intersection" of DM and HF. Today, the increasing interest and concern have caused DMC to be revisited and the first step in controlling the chaos around DMC is to organize and analyze all of the available evidence from preclinical and clinical studies. This review aims to illustrate the current concepts of DMC by shedding light on the new molecular mechanisms. (Circ J 2014; 78: 576-583).

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“…Thus, BK-2R expression was downregulated during the process, which leads to end-stage heart failure, while the expression of BK-1R was upregulated [1]. Immunohistochemical studies of the heart revealed that the differential expression of BK-Rs appears to be primarily confined to endothelial cells of the small intramyocardial coronary vessels, whose dysfunction has been linked to other disease conditions, such as hypertension [2], type 2 diabetes [3] and type 1 diabetes [4]. Indeed, myocardial ischemia due to dysfunction of the microvascular coronary endothelium [5] is a central pathophysiological feature leading to hypertrophic or dilated cardiomyopathy, and ultimately to manifest heart failure [6,7,8].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of Bradykinin Type 2 Receptor Expression in Cardiac Endothelial Cells during Senescence

Nurmi

Heikkilä

Vapaatalo³

et al. 2011

J Vasc Res

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Objectives: Bradykinin type 2 receptor (BK-2R) knockout mice develop microvascular dysfunction and cardiac hypertrophy. In aged human cardiac microvascular endothelium, dysfunction develops before heart failure symptoms. Since endothelial aging is an independent risk factor for cardiovascular disease, we aimed to clarify the role of kinin receptors in age-related endothelial senescence. Methods and Results: Using qRT-PCR, a downregulation of BK-2Rs during senescence of cultured human coronary artery endothelial cells (HCAECs) and rat cardiac microvascular endothelial cells (RCMECs) was observed. BK-2R downregulation was associated with a decreased cell proliferation rate, with a growth arrest phenotype and reduced angiogenic potential. By staining senescence-associated β-galactosidase, RCMECs from old spontaneously hypertensive rats (SHRs) were found to be significantly more senescent than those derived from age-matched WKY rats, albeit their telomere lengths were similar. Despite downregulation of BK-2Rs and BK-1Rs, a novel family member GPR-100 was highly expressed in HCAECs throughout the culture period. Conclusions: Aging cardiac endothelial cells gradually lose their capacity to express BK-2Rs, and this loss appears to be parallel with a loss of the angiogenic potential of the aging cells. Since RCMECs from hypertensive rats showed premature senescence, hypertension may predispose to cardiac dysfunction by accelerating endothelial aging.

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Diastolic dysfunction and abnormalities of the microcirculation in type 2 diabetes

Cited by 64 publications

References 45 publications

Association between High-Sensitivity C-Reactive Protein and Left Ventricular Diastolic Function Assessed by Echocardiography in Patients with Cardiovascular Risk Factors

Association between High-Sensitivity C-Reactive Protein and Left Ventricular Diastolic Function Assessed by Echocardiography in Patients with Cardiovascular Risk Factors

Diabetes-Related Heart Failure

Downregulation of Bradykinin Type 2 Receptor Expression in Cardiac Endothelial Cells during Senescence

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