Patterns of left ventricular remodeling in patients with Duchenne Muscular Dystrophy: a cardiac MRI study of ventricular geometry, global function, and strain

AbstractBackground and aims. Aortic sclerosis associates an increased risk of cardiovascular morbidity and mortality. Recent studies suggest that aortic sclerosis is able to produce ventricular remodeling through inflammatory, non-hemodynamic mechanisms. Our study aims to evaluate the correlation between ventricular remodeling and aortic sclerosis severity.Method. 68 patients with aortic sclerosis without other signifficant associated valvulopathies were examined clinically, biologically and echocardiographic. In 20 patients, we quantiffied the severity of aortic valve calciffication using the backscatter ecographic technique, in parasternal long and short axis view. Backscatter values obtained at the valvular level were calibrated to the blood and pericardium backscatter values.Results. In the 68 patients group, transvalvular aortic velocity correlates with left ventricular mass (p =0.031), which in turn incline to augment with increasing calciffication severity assessed by backscatter. Calciffication severity assessed by backscatter corellates with transvalvular aortic velocity in parasternal long axis view (p =0.039 for blood calibrated backscatter, p =0.029 for pericardium calibrated backscatter), and tends to augment with increasing transvalvular aortic velocity in parasternal short axis view. Patients with normal ventricular geometry incline to have lower aortic transvalvular velocities and a lower degree of calciffication (evaluated by backscatter) compared to patients with ventricular remodeling.Conclusions. Aortic sclerosis is not benign, and may lead, in time, to left ventricular remodeling. With the progression of valvular calciffications in aortic sclerosis patients, the prevalence of ventricular remodeling tends to increase.

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Serial quantification of myocardial infarction tissue heterogeneity during infarct healing by cardiac MRI provides strong characterization of left ventricular remodeling (the NHLBI PROSPECT-CMR Study)

Journal of Cardiovascular Magnetic Resonance ◽

10.1186/1532-429x-13-s1-o65 ◽

2011 ◽

Vol 13 (S1) ◽

Author(s):

Bobby Heydari ◽

Shuaib M Abdullah ◽

Otavio Coelho-Filho ◽

François-Pierre Mongeon ◽

Harris Alanna ◽

...

Keyword(s):

Myocardial Infarction ◽

Cardiac Mri ◽

Ventricular Remodeling ◽

Left Ventricular Remodeling ◽

Left Ventricular ◽

Tissue Heterogeneity ◽

Infarct Healing

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Multiparametric PET and MRI of myocardial damage after myocardial infarction: correlation of integrin αvβ3 expression and myocardial blood flow

European Journal of Nuclear Medicine and Molecular Imaging ◽

10.1007/s00259-020-05034-z ◽

2020 ◽

Author(s):

Marcus R. Makowski ◽

Christoph Rischpler ◽

Ullrich Ebersberger ◽

Alexandra Keithahn ◽

Markus Kasel ◽

...

Keyword(s):

Myocardial Infarction ◽

Blood Flow ◽

Myocardial Blood Flow ◽

Cardiac Mri ◽

Ventricular Remodeling ◽

Left Ventricular Remodeling ◽

Left Ventricular ◽

Myocardial Segment ◽

Αvβ3 Integrin ◽

Pet Ct

Abstract Purpose Increased angiogenesis after myocardial infarction is considered an important favorable prognostic parameter. The αvβ3 integrin is a key mediator of cell-cell and cell-matrix interactions and an important molecular target for imaging of neovasculature and repair processes after MI. Thus, imaging of αvβ3 expression might provide a novel biomarker for assessment of myocardial angiogenesis as a prognostic marker of left ventricular remodeling after MI. Currently, there is limited data available regarding the association of myocardial blood flow and αvβ3 integrin expression after myocardial infarction in humans. Methods Twelve patients were examined 31 ± 14 days after MI with PET/CT using [18F]Galacto-RGD and [13N]NH3 and with cardiac MRI including late enhancement on the same day. Normal myocardium (remote) and areas of infarction (lesion) were identified on the [18F]Galacto-RGD PET/CT images by correlation with [13N]NH3 PET and cardiac MRI. Lesion/liver-, lesion/blood-, and lesion/remote ratios were calculated. Blood flow and [18F]Galacto-RGD uptake were quantified and correlated for each myocardial segment (AHA 17-segment model). Results In 5 patients, increased [18F]Galacto-RGD uptake was notable within or adjacent to the infarction areas with a lesion/remote ratio of 46% (26–83%; lesion/blood 1.15 ± 0.06; lesion/liver 0.61 ± 0.18). [18F]Galacto-RGD uptake correlated significantly with infarct size (R = 0.73; p = 0.016). Moreover, it correlated significantly with restricted blood flow for all myocardial segments (R = − 0.39; p < 0.0001) and even stronger in severely hypoperfused areas (R = − 0.75; p < 0.0001). Conclusion [18F]Galacto-RGD PET/CT allows the visualization and quantification of myocardial αvβ3 expression as a key player in angiogenesis in a subset of patients after MI. αvβ3 expression was more pronounced in patients with larger infarcts and was generally more intense but not restricted to areas with more impaired blood flow, proving that tracer uptake was largely independent of unspecific perfusion effects. Based on these promising results, larger prospective studies are warranted to evaluate the potential of αvβ3 imaging for assessment of myocardial angiogenesis and prediction of ventricular remodeling.

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Abstract 3634: Association of Weight Loss and Changes in Left Ventricular Geometry and Function - Results of the longitudinal population based MONICA/KORA-Survey

Circulation ◽

10.1161/circ.116.suppl_16.ii_824-c ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Jan Stritzke ◽

Marcello R Markus ◽

Wolfgang Lieb ◽

Andreas Luchner ◽

Angela Döring ◽

...

Keyword(s):

Weight Loss ◽

Body Weight ◽

Weight Gain ◽

Ventricular Remodeling ◽

Left Ventricular Remodeling ◽

Left Ventricular ◽

Left Ventricular Geometry ◽

Ventricular Geometry ◽

And Function

Background: Obesity is related to left ventricular (LV) hypertrophy and diastolic dysfunction. However it remains unclear if changes in life style resulting in loss of body weight also have beneficial effects on left ventricular remodeling. In this study we evaluated the effects of weight loss on left ventricular geometry and function during ten years of follow-up. Methods: Subjects (n=1005, aged 25 to 74 years) who originated from a gender and age stratified random sample of German residents of the Augsburg area were examined by standardized echocardiography at baseline and again after ten years. The associations between weight loss and long-term changes of left ventricular end-diastolic diameter (LVEDD), wall thickness (WT), left ventricular mass (LVM), and left atrial diameter (LA) were assessed. Mean relative changes and odds ratios were computed by statistical models adjusting for gender, age, body height, systolic blood pressure and body weight at baseline. Results: After ten years of follow-up 305 individuals presented with a loss of body weight (−3.5+/−3.4kg on average). Whereas 700 subjects presented with an increase of body weight (+5.4+/−4.7kg). Ageing related changes in LV geometry were significantly different in the two groups. Specifically, individuals with weight loss displayed a favorable geometry with relative changes of WT (+5.9% [CI-95% 4.3, 7.5] vs. + 8.1% [7.0, 9.2], p=0.024), LVEDD (−0.6% [−1.5, 0.2] vs. 30.8% [0.2, 1.4], p=0.008), LVM (+6.5% [4.3, 8.8] vs. +11.9% [10.4, 13.5], p<0.001) and LA (−0.9% [−2.1, 0.2] vs. +2.5% [1.7, 3.3], p<0.001), as compared to individuals with weight gain. Moreover, the risk for incident left ventricular hypertrophy (OR 2.5 [1.5– 4.3], p=0.001) and incident diastolic dysfunction (OR 1.9 [1.1–3.4], p=0.023) was significantly higher in individuals presenting with an increase in body weight. Conclusions: As compared to weight gain, weight loss is associated with a significant deceleration of left ventricular remodeling during ageing of the heart. Nevertheless, even in the weight loss group there was no regression in left ventricular mass detectable. Consequently, early interventions especially in young obese individuals are essential for prevention of premature onset of cardiac remodeling.

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