To investigate the relation between myocardial perfusion and heart failure (HF) status after revascularisation in patients with HF due to hibernating myocardium (HM) in diabetic and non-diabetic subjects.
31 diabetic and 33 non-diabetic subjects with HF due to HM, who were already scheduled for complete revascularisation, were studied. Before and after revascularisation, left ventricular function and regional perfusion in subendocardial and subepicardial portions of the left ventricular wall were evaluated.
Before revascularisation, left ventricular function and regional perfusion were similar in diabetic and non-diabetic subjects. At 6 months after revascularisation, subepicardial perfusion was markedly improved both in diabetic and non-diabetic subjects. However, subendocardial perfusion was markedly improved only in non-diabetic subjects and was little changed in diabetic patients. Thus, subendocardial perfusion was much lower in diabetic than non-diabetic subjects. Left ventricular function was improved more in non-diabetic than in diabetic subjects. Persistent HF was found much more often in diabetic than non-diabetic subjects. At multivariate analysis, subendocardial perfusion at 6 months independently contributed to persistent HF.
This study describes the intramural heterogeneity of recovery of myocardial perfusion with depressed improvement in the subendocardial portion and its relation with persistent HF after complete revascularisation in diabetic patients with HF due to HM.
"In particular, severe myocardial ischemia was found in 46% of patients with and in 27% of those without post-stress LVEF drop. Several studies reported that in patients with suspected or known CAD stress-induced transient LV dysfunction is associated with severe and extensive ischemia [3-7,31,32]. However, these studies evaluated post-stress LVEF drop in unselected patients population. "
[Show abstract][Hide abstract] ABSTRACT: To evaluate the relevance of stress-induced decrease in left ventricular ejection fraction (LVEF) in patients with type-2 diabetes.
A total of 684 diabetic patients with available rest and post-stress gated myocardial perfusion single-photon emission computed tomography (MPS) data were enrolled. An automated algorithm was used to determine the perfusion scores using a 17-segment model. LVEF drop was considered significant if the post-stress LVEF was >=5% below the rest value. Follow-up data were available in 587 patients that were followed for the occurrence of cardiac death, nonfatal myocardial infarction, or unstable angina requiring revascularization.
A post-stress LVEF drop >=5% was observed in 167 (24%) patients. Patients with LVEF drop had higher summed stress score (p < 0.05), summed difference score (p < 0.001), and rest LVEF (p < 0.001) compared to patients without. Conversely, summed rest score, a measure of infarct size, was comparable between the two groups. At multivariable analysis, summed difference score and rest LVEF were independent predictors (both p < 0.001) of post-stress LVEF drop. Myocardial perfusion was abnormal in 106 (63%) patients with post-stress LVEF drop and in 296 (57%) of those without (p = 0.16). The overall event-free survival was lower in patients with post-stress LVEF drop than in those without (log rank chi2 7.7, p < 0.005). After adjusting for clinical data and MPS variables, the hazard ratio for cardiac events for post-stress LVEF drop was 1.52 (p < 0.01).
In diabetic patients stress-induced ischemia is an independent predictor of post-stress LVEF drop; however, a reduction in LVEF is detectable also in patients with normal perfusion. Finally, post-stress LVEF drop increase the risk of subsequent cardiac events in diabetic patients.
"This may be the consequence of an overall and homogeneous myocardial injury. Because subendocardial longitudinal fibres are the most vulnerable in pathological conditions, we deliberately focused our analysis on longitudinal deformation . Longitudinal strain is the most reliable and studied parameter of deformation modalities and the comparison of radial strain results in diabetic populations is not reliable among different studies [25,40]. "
[Show abstract][Hide abstract] ABSTRACT: Aims
Although dipyridamole is a widely used pharmacological stress agent, the direct effects on myocardium are not entirely known. Diabetic cardiomyopathy can be investigated by 2D-strain echocardiography. The aim of this study was to assess myocardial functional reserve after dipyridamole infusion using speckle-tracking echocardiography.
Seventy-five patients referred for dipyridamole stress myocardial perfusion gated SPECT (MPGS) were examined by echocardiography to assess a new concept of longitudinal strain reserve (LSR) and longitudinal strain rate reserve (LSRR) respectively defined by the differences of global longitudinal strain (GLS) and longitudinal strain rate between peak stress after dipyridamole and rest. Twelve patients with myocardial ischemia were excluded on the basis of MPGS as gold standard.
Mean LSR was −2.28±2.19% and was more important in the 28 (44%) diabetic patients (−3.27±1.93%; p = 0.001). After multivariate analyses, only diabetes improved LSR (p = 0.011) after dipyridamole infusion and was not associated with glycaemic control (p = 0.21), insulin therapy (p = 0.46) or duration of the disease (p = 0.80). Conversely, age (p = 0.002) remained associated with a decrease in LSR. LSSR was also correlated to age (p = 0.005). Patients with a LSR < 0% have a better survival after 15 months (log-rank p = 0.0012).
LSR explored by 2D speckle-tracking echocardiography after dipyridamole infusion is a simple and new concept that provides new insights into the impact of diabetes and age on the myocardium with a potential prognostic value.
[Show abstract][Hide abstract] ABSTRACT: Diabetes and its complications are a major public health burden in the developed world. The major cause of diabetic complications is abnormal growth of new blood vessels. This dysfunctional neovascularization results in significant morbidity and mortality in patients with diabetes and, as such, is a major focus of basic and clinical investigation. It has become clear that hyperglycemia disrupts tissue-level signaling in response to hypoxia and ischemia, impairs the vasculogenic potential of circulating stem cells and fundamentally alters the structure and function of key neovascularization proteins, including hypoxia-inducible factor-1. These mechanistic and pathophysiologic studies have revealed new therapeutic targets to restore normal neovascularization and to ameliorate and prevent diabetic vascular complications.
Expert Review of Endocrinology & Metabolism 12/2009; 5(1):99-111. DOI:10.1586/eem.09.57
Jordan J. Lancaster, Elizabeth Juneman, Pablo Sanchez, Kyle Weigand, Talal Moukabary, Nicole Lahood, Joseph J. Bahl, Steven Goldman
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