scholarly journals Prophylactic, single-drug cardioprotection in a comparative, experimental study of doxorubicin-induced cardiomyopathy

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Mária Lódi ◽  
Viktor Bánhegyi ◽  
Beáta Bódi ◽  
Alexandra Gyöngyösi ◽  
Árpád Kovács ◽  
...  
Keyword(s):  
Enzyme Inhibitor ◽  
Primary Prophylaxis ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Common Side Effect ◽  
Serum Samples ◽  
Ventricular Ejection Fraction ◽  
Oncological Patients ◽  
Male Wistar Rats

Abstract Background Cardiomyopathy is a common side effect of doxorubicin (DOX) chemotherapy. Despite intensive research efforts in the field, there is still no evidence available for routine cardioprotective prophylaxis to prevent cardiotoxicity in the majority of oncological patients at low risk of cardiovascular disease. We have recently demonstrated the advantages of a prophylactic, combined heart failure therapy in an experimental model of DOX-induced cardiomyopathy. In the current work, we focus on individually applied prophylactic medications studied in the same translational environment to clarify their distinct roles in the prevention of DOX cardiotoxicity. Methods Twelve-week-old male Wistar rats were divided into 5 subgroups. Prophylactic β-blocker (BB, bisoprolol), angiotensin-converting enzyme inhibitor (ACEI, perindopril) or aldosterone antagonist (AA, eplerenone) treatments were applied 1 week before DOX administration, then 6 cycles of intravenous DOX chemotherapy were administered. Rats receiving only intravenous DOX or saline served as positive and negative controls. Blood pressure, heart rate, body weight, and echocardiographic parameters were monitored in vivo. Two months after the last DOX administration, the animals were sacrificed, and their heart and serum samples were frozen in liquid nitrogen for histological, mechanical, and biochemical measurements. Results All prophylactic treatments increased the survival of DOX-receiving animals. The lowest mortality rates were seen in the BB and ACEI groups. The left ventricular ejection fraction was only preserved in the BB group. The DOX-induced increase in the isovolumetric relaxation time could not be prevented by any prophylactic treatment. A decreased number of apoptotic nuclei and a preserved myocardial ultrastructure were found in all groups receiving prophylactic cardioprotection, while the DOX-induced fibrotic remodelling and the increase in caspase-3 levels could only be substantially prevented by the BB and ACEI treatments. Conclusion Primary prophylaxis with cardioprotective agents like BB or ACEI has a key role in the prevention of DOX-induced cardiotoxicity in healthy rats. Future human studies are necessary to implement this finding in the clinical management of oncological patients free of cardiovascular risk factors.

Electrophysiologic properties and ventricular fibrillation in normal and myopathic hearts

1999 ◽  
Vol 77 (7) ◽  
pp. 510-519 ◽  
Author(s):  
Katherine M Kavanagh ◽  
Patricia A Guerrero ◽  
Bodh I Jugdutt ◽  
Francis X Witkowski ◽  
Jeffrey E Saffitz
Keyword(s):  
Ventricular Fibrillation ◽  
Myocardial Dysfunction ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Functional Abnormality ◽  
Ventricular Ejection Fraction ◽  
Anisotropic Properties

This study tests the hypothesis that moderate myocardial dysfunction is associated with altered myocardial anisotropic properties and structurally altered ventricular fibrillation (VF). Mongrel dogs were randomized to either a control group or a group that was rapidly paced at 250 beats/min until the left ventricular ejection fraction was [Formula: see text] 40%. Changes in anisotropic properties and the electrical characteristics of VF associated with the development of moderate myocardial dysfunction were assessed by microminiature epicardial mapping studies. In vivo conduction, refractory periods, and repolarization times were prolonged in both longitudinal and transverse directions in myopathic animals versus controls. VF was different in myopathic versus control animals. There were significantly more conducted deflections during VF in normal hearts compared with myopathic hearts. Propagated deflection-to-deflection intervals during VF were significantly longer in myopathic hearts compared with controls (125.5 ± 49.06 versus 103.4 ± 32.9 ms, p = 0.009). There were no abnormalities in cell size, cell shape, or the number of intercellular gap junctions and there was no detectable change in the expression of the gap junction proteins Cx43 and Cx45. Moderate myocardial dysfunction is associated with significant electrophysiological abnormalities in the absence of changes in myocardial cell morphology or intercellular connections, suggesting a functional abnormality in cell-to-cell communication.Key words: cardiomyopathy, anisotropy, fibrillation, defibrillation.

Abstract 165: The 18 kDa FGF-2 Prevents the Doxorubicin-induced Cardiac Damage and Amp-activated Kinase Activation, in vitro and in vivo

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Navid Koleini ◽  
Jon Jon Santiago ◽  
Barbara E Nickel ◽  
Robert Fandrich ◽  
Davinder S Jassal ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Cell Death ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Wild Type ◽  
Rat Cardiomyocytes ◽  
Ventricular Ejection Fraction ◽  
Compound C

Introduction: Protection of the heart from chemotherapeutic (Doxorubicin, DOX) drug-induced toxicity is a desirable goal, to limit side effects of cancer treatments. DOX toxicity has been linked to the activation (phosphorylation) of the AMP-activated kinase, AMPK. The 18 kDa low molecular weight isoform of fibroblast growth factor 2 (Lo-FGF-2) is a known cardioprotective and cytoprotective agent. In this study we have tested the ability of Lo-FGF-2 to protect from DOX-induced damage in rat cardiomyocytes in vitro, and in transgenic mouse models in vivo, in relation to AMPK activation. Methods: Rat neonatal cardiomyocytes in culture were exposed to DOX (0.5 μM) in the presence or absence of pre-treatment Lo-FGF-2 (10 ng/ml). Compound C was used to block phosphorylation (activity) of AMPK. Levels of cell viability/death (using Calcein-AM/Propidium iodide assay), phospho -and total AMPK, and apoptotic markers such as active caspase 3 were analyzed. In addition, transgenic mice expressing only Lo-FGF2, and wild type mice, expressing both high molecular weight (Hi-FGF2) as well as Lo-FGF2 were subjected to DOX injection (20 mg/kg, intraperitoneal); echocardiography was used to examine cardiac function at baseline and at 10 days post-DOX. Results: DOX-induced cell death of cardiomyocytes in culture was maximal at 24 hours post-DOX coinciding with significantly increased in activated (phosphorylated) AMPK. Compound C attenuated DOX-induced cardiomyocyte loss. Pre-incubation with Lo-FGF-2 decreased DOX induced cell death, and also attenuated the phosphorylation of AMPK post-DOX. Relative levels of phospho-AMPK were lower in the hearts of Lo-FGF2-expressing male mice compared to wild type. DOX-induced loss of contractile function (left ventricular ejection fraction and endocardial velocity) was negligible in Lo-FGF2-expressing mice but significant in wild type mice. Conclusion: Lo-FGF-2 protects the heart from DOX-induced damage in vitro and in vivo, by a mechanism likely involving an attenuation of AMPK activity.

scholarly journals Clinical profile and management of patients with incident and recurrent acute myocardial infarction in Albania - a call for more focus on prevention strategies

2017 ◽  
Vol 56 (4) ◽  
pp. 236-243
Author(s):  
Sokol Myftiu ◽  
Enxhela Sulo ◽  
Genc Burazeri ◽  
Bledar Daka ◽  
Ilir Sharka ◽  
...  
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Enzyme Inhibitor ◽  
Left Ventricular ◽  
Clinical Profile ◽  
Left Ventricular Ejection ◽  
Hospital Treatment ◽  
Ventricular Ejection Fraction ◽  
Incident Cases

AbstractBackgroundThe clinical profile of acute myocardial infarction (AMI) patients reflects the burden of risk factors in the general population. Differences between incident (first) and recurrent (repeated) events and their impact on treatment are poorly described. We studied potential differences in the clinical profile and in-hospital treatment between patients hospitalised with an incident and recurrent AMI.MethodsA total of 324 patients admitted in the Coronary Care Unit of ‘Mother Teresa’ hospital, Tirana, Albania (2013-2014), were included in the study. Information on AMI type, complications and risk factors was obtained from patient’s medical file.Logistic regression analyses were used to explore differences between the incident and recurrent AMIs regarding clinical profile and in-hospital treatment.ResultsOf all patients, 50 (15.4%) had a prior AMI. Compared to incident cases, recurrent cases were older (P=0.01), more often women (P=0.01), less educated (P=0.01), and smoked less (P=0.03). Recurrent cases experienced more often heart failure (HF) (OR=2.48; 95% CI: 1.31–4.70), impaired left ventricular ejection fraction (OR=1.97; 95% CI:1.05–3.71), and multivessel disease (OR=6.32; 95% CI: 1.43–28.03) than incident cases. In-hospital use of beta-blockers was less frequent among recurrent compared to incident cases (OR=0.45; 95% CI: 0.24–0.85), while no statistically significant differences between groups were observed regarding angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, statin, aspirin or invasive procedures.ConclusionA more severe clinical expression of the disease and underutilisation of treatment among recurrent AMIs are likely to explain their poorer prognosis compared to incident AMIs.

scholarly journals Bone marrow-derived stromal cells home to and remain in the infarcted rat heart but fail to improve function: an in vivo cine-MRI study

2008 ◽  
Vol 295 (2) ◽  
pp. H533-H542 ◽  
Author(s):  
Carolyn A. Carr ◽  
Daniel J. Stuckey ◽  
Louise Tatton ◽  
Damian J. Tyler ◽  
Sarah J. M. Hale ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Therapy ◽  
Cardiac Function ◽  
Stromal Cells ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Cine Mri ◽  
Iron Oxide Particles ◽  
Ventricular Ejection Fraction

Basic and clinical studies have shown that bone marrow cell therapy can improve cardiac function following infarction. In experimental animals, reported stem cell-mediated changes range from no measurable improvement to the complete restoration of function. In the clinic, however, the average improvement in left ventricular ejection fraction is around 2% to 3%. A possible explanation for the discrepancy between basic and clinical results is that few basic studies have used the magnetic resonance (MR) imaging (MRI) methods that were used in clinical trials for measuring cardiac function. Consequently, we employed cine-MR to determine the effect of bone marrow stromal cells (BMSCs) on cardiac function in rats. Cultured rat BMSCs were characterized using flow cytometry and labeled with iron oxide particles and a fluorescent marker to allow in vivo cell tracking and ex vivo cell identification, respectively. Neither label affected in vitro cell proliferation or differentiation. Rat hearts were infarcted, and BMSCs or control media were injected into the infarct periphery ( n = 34) or infused systemically ( n = 30). MRI was used to measure cardiac morphology and function and to determine cell distribution for 10 wk after infarction and cell therapy. In vivo MRI, histology, and cell reisolation confirmed successful BMSC delivery and retention within the myocardium throughout the experiment. However, no significant improvement in any measure of cardiac function was observed at any time. We conclude that cultured BMSCs are not the optimal cell population to treat the infarcted heart.

scholarly journals miR-19a-3p containing exosomes improve function of ischaemic myocardium upon shock wave therapy

2019 ◽  
Vol 116 (6) ◽  
pp. 1226-1236 ◽  
Author(s):  
Can Gollmann-Tepeköylü ◽  
Leo Pölzl ◽  
Michael Graber ◽  
Jakob Hirsch ◽  
Felix Nägele ◽  
...  
Keyword(s):  
Shock Wave ◽  
Myocardial Fibrosis ◽  
Myocardial Ischaemia ◽  
Heart Function ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Shock Wave Therapy ◽  
Ventricular Ejection Fraction ◽  
Ischaemic Myocardium

Abstract Aims As many current approaches for heart regeneration exert unfavourable side effects, the induction of endogenous repair mechanisms in ischaemic heart disease is of particular interest. Recently, exosomes carrying angiogenic miRNAs have been described to improve heart function. However, it remains challenging to stimulate specific release of reparative exosomes in ischaemic myocardium. In the present study, we sought to test the hypothesis that the physical stimulus of shock wave therapy (SWT) causes the release of exosomes. We aimed to substantiate the pro-angiogenic impact of the released factors, to identify the nature of their cargo, and to test their efficacy in vivo supporting regeneration and recovery after myocardial ischaemia. Methods and results Mechanical stimulation of ischaemic muscle via SWT caused extracellular vesicle (EV) release from endothelial cells both in vitro and in vivo. Characterization of EVs via electron microscopy, nanoparticle tracking analysis and flow cytometry revealed specific exosome morphology and size with the presence of exosome markers CD9, CD81, and CD63. Exosomes exhibited angiogenic properties activating protein kinase b (Akt) and extracellular-signal regulated kinase (ERK) resulting in enhanced endothelial tube formation and proliferation. A miRNA array and transcriptome analysis via next-generation sequencing were performed to specify exosome content. miR-19a-3p was identified as responsible cargo, antimir-19a-3p antagonized angiogenic exosome effects. Exosomes and target miRNA were injected intramyocardially in mice after left anterior descending artery ligation. Exosomes resulted in improved vascularization, decreased myocardial fibrosis, and increased left ventricular ejection fraction as shown by transthoracic echocardiography. Conclusion The mechanical stimulus of SWT causes release of angiogenic exosomes. miR-19a-3p is the vesicular cargo responsible for the observed effects. Released exosomes induce angiogenesis, decrease myocardial fibrosis, and improve left ventricular function after myocardial ischaemia. Exosome release via SWT could develop an innovative approach for the regeneration of ischaemic myocardium.

Abstract 242: Subcutaneous and Visceral Adipose-Derived Stem Cells Have Similar Biological Properties and Both Improve Cardiac Function of Infarcted Rat Hearts

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Chao Chi ◽  
Bo Xiang ◽  
Jixian Deng ◽  
Fei Wang ◽  
Kanmani Natarajan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cardiac Function ◽  
Formation Rate ◽  
Biological Properties ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Ventricular Ejection Fraction ◽  
Visceral Adipose

Background: Adipose stem cells (ASC) from subcutaneous and visceral adipose tissues have been studied individually. However, it is unclear whether ASC from the two sources have different biological properties and, more importantly, whether one sub-type of ASC is more effective in treatment of CHF. This study was designed to address these concerns. Methods: Morphology, yield, proliferation, surface markers, and cytokine secretion of rat subcutaneous ASC (S-ASC) and visceral ASC (V-ASC) were analyzed. A rat model of myocardial infarction (MI) was established by occlusion of the LAD. 7 days after MI, S-ASC (n = 11), V-ASC (n = 11), and cell culture medium (Control, n = 7) were injected into the infarct rim, respectively. Cardiac function of the infarcted hearts was monitored with MRI for 6 months. Results: Both S-ASC and V-ASC exhibited a fibroblast-like morphology and expressed stromal cell markers (CD29, CD90 and CD105). No significant expression of hematopoietic markers (CD11b, CD34 and CD45) was found. Under appropriate conditions, both cells could differentiate to adipocyte- and osteocyte-like cells. Both of them expressed a significant level of HGF, IGF-1 and VEGF. As to their differences, V-ASC had approximately 3-times greater cell yield and a lower colony-formation rate (9.8±1.0% vs.13.5±2.6%) relative to S-ASC. In contrast, S-ASC showed a significantly greater growth rate (Doubling Time: 17.9 h vs. 26.0 h) relative to V-ASC. Both S-ASC and V-ASC-treated hearts showed a significantly greater left ventricular ejection fraction (LVEF, 58.3% and 56.7%) than the control group (LVEF, 47.2%) at end of 6 months. LVEF between the two ASC-treated groups was not significantly different. Finally, the implanted stem cells were readily detected in vivo with MRI for at least 6 months. Myocardial tissue sections showed existence of ASC and their locations matched with MRI signals. Conclusions: S-ASC and V-ASC share several biological characteristics. Both provide comparable significant improvement on cardiac function. Moreover, these implanted cells can be reliably tracked for at least 6 months using MRI. We conclude that the S-ASC and V-ASC are equally effective for treatment of heart failure.

Plasma concentration of Fas/Fas ligand and left ventricular function in response to metoprolol in conjunction with standard treatment

2007 ◽  
Vol 112 (5) ◽  
pp. 299-304 ◽  
Author(s):  
Yuan-ping Hou ◽  
Jin-ling Wu ◽  
Qian Fan ◽  
Miao-bing Liu ◽  
Bao-ling Yin ◽  
...  
Keyword(s):  
Fas Ligand ◽  
Ace Inhibitor ◽  
Standard Treatment ◽  
Enzyme Inhibitor ◽  
Plasma Concentrations ◽  
Left Ventricular ◽  
Treatment Regime ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Soluble Fas

Recent studies suggest that cardiac myocyte apoptosis contributes to the progress of CHF (congestive heart failure). In the present study, we tested the hypothesis that metoprolol in conjunction with the standard treatment regime for CHF [an ACE (angiotensin-converting enzyme) inhibitor, diuretics and digoxin] may significantly reduce the plasma concentrations of the apoptotic mediators sFas (soluble Fas) and sFasL (soluble Fas ligand) in patients with CHF. An ELISA was used to determine the plasma concentrations of sFas and sFasL in 106 patients with stable CHF at recruitment. Echocardiography was performed at baseline and after 1 year of treatment with metoprolol in conjunction with the standard treatment regime for CHF (i.e. an ACE inhibitor, diuretics and digoxin). The dose of metoprolol was doubled on a biweekly basis up to 50 mg twice a day or maintained at the maximum tolerated dose. Data after 1 year were available for 92 patients and were analysed. The plasma concentrations of sFas and sFasL in patients with CHF decreased significantly (P<0.01) after 1 year of treatment with metoprolol in conjunction with the standard treatment regime compared with at baseline (5.4±0.2 compared with 3.2±0.1 ng/ml respectively for sFas, and 52.1±2.3 compared with 26.7±1.0 pg/ml respectively for sFasL). Compared with baseline, after 1 year of treatment with metoprolol in conjunction with the standard treatment regime there were significant improvements in LV (left ventricular) ejection fraction (from 32.6±0.9 to 51.5±0.8%; P<0.01), LV end-diastolic dimension (from 69.8±0.6 to 57.7±0.3 mm; P<0.01), LV end-systolic dimension (from 53.9±0.6 to 40.5±0.5 mm; P<0.01), LV end-diastolic volume (from 254.7±5.0 to 164.1±2.2 ml; P<0.01) and LV end-systolic volume (from 142.0±4.2 to 72.2±2.0 ml; P<0.01). In addition, the distance walked in a 6-min walk test increased markedly (P<0.01) from 260.3±5.2 m at baseline to 440.9±5.7 m after 1 year of treatment. In conclusion, we have demonstrated that metoprolol in conjunction with an ACE inhibitor, diuretics and digoxin in patients with CHF can lead to a reverse in LV remodelling potentially through its anti-apoptotic effects.

scholarly journals Nicorandil Ameliorates Doxorubicin-Induced Cardiotoxicity in Rats, as Evaluated by 7 T Cardiovascular Magnetic Resonance Imaging

2021 ◽  
Author(s):  
Yixuan Wan ◽  
Bo He ◽  
Dongyong Zhu ◽  
Lei Wang ◽  
Ruijue Huang ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Cardiac Function ◽  
T2 Mapping ◽  
Myocardial Strain ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Common Side Effect ◽  
Sprague Dawley ◽  
Ventricular Ejection Fraction ◽  
Doxorubicin Group

Abstract Purpose Doxorubicin-induced cardiotoxicity (DIC) is a common side effect of doxorubicin chemotherapy, and a major mechanism of DIC is inflammation. However, no effective method exists to prevent DIC. In the present study, we investigated the cardioprotective effects of nicorandil against DIC using multiparametric cardiac magnetic resonance (CMR) imaging and elucidated the anti-inflammatory properties of nicorandil in rat models. Methods Male Sprague-Dawley rats received four weekly intraperitoneal doxorubicin doses (4 mg/kg/injection) to establish the DIC model. After treatment with or without nicorandil (3 mg/kg/day) or diazoxide (10 mg/kg/day) orally, all the groups underwent weekly CMR examinations, including cardiac function and strain assessment and T2 mapping, for 6 weeks. Additionally, blood samples and hearts were collected to examine inflammation and histopathology. Results According to our results, the earliest DIC CMR parameter in the doxorubicin group was T2 mapping time prolongation compared with the DIC rats treated with nicorandil (doxorubicin+nicorandil group) at week 2. Subsequently, the left ventricular ejection fraction (LVEF) and global peak systolic myocardial strain in the doxorubicin group were significantly reduced, and nicorandil effectively inhibited these effects at week 6. Our results were confirmed by histopathological evaluations. Furthermore, nicorandil treatment had a protective effect against the doxorubicin-induced inflammatory response. Interestingly, similar protective results were obtained using the KATP channel opener diazoxide. Conclusion Collectively, our findings indicate that nicorandil application ameliorates DIC in rats with significantly higher cardiac function and myocardial strain and less fibrosis, apoptosis and inflammatory cytokine production. Nicorandil prevents T2 abnormalities in the early stages of DIC, showing a high clinical value for early nicorandil treatment in chemotherapy patients.

Abstract 11882: Comprehensive Hemodynamic Analysis of Coronary Arterial Responses to Acetylcholine Provocation Test in Patients With Coronary Vasospastic Angina

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Kenshi Yamanaga ◽  
Kenichi Tsujita ◽  
Naohiro Komura ◽  
Kenji Sakamoto ◽  
Masanobu Ishii ◽  
...  
Keyword(s):  
Provocation Test ◽  
Left Ventricular ◽  
Coronary Vasospasm ◽  
Vasospastic Angina ◽  
Left Ventricular Ejection ◽  
Doppler Velocity ◽  
Ventricular Ejection Fraction ◽  
Flow Reserve ◽  
Dual Sensor

Introduction: Whereas our prior study showed diffuse coronary intimal thickening in pts with coronary vasospastic angina (VSA), coronary epicardial and microvascular (MV) hemodynamic and vessel response during coronary vasospasm has not been well studied. Hypothesis: We hypothesized that coronary pathogenic abnormalities responsible for coronary vasospasm may not be confined to coronary epicardial spastic segments, but the hemodynamic abnormalities may exist in the entire coronary bed. Methods: According to acetylcholine (ACh) provocation tests, excluding pts with atherosclerotic coronary obstruction (stenosis >50% diameter) and possible heart failure (left ventricular ejection fraction <50%), 41 pts were divided into 2 groups; VSA group (n=20) and non-VSA group (n=21). To evaluate hemodynamic parameters comprehensively, average peak velocity (APV), coronary blood flow (CBF: π (APV/2)(vessel diameter/2) 2 ), hyperemic MV resistance (hMR), coronary vascular resistance (CVR: Pd/CBF) and coronary distal pressure (Pd) were measured continuously utilizing a dual-sensor (Doppler velocity and pressure)-equipped guidewire (Combowire, Volcano Therapeutics, Inc.) during ACh provocation test. Results: There were no differences between the 2 groups in baseline characteristics. In spite of absence of between-group differences at baseline in CBF (55±26 vs. 51±29, p=0.5) and CVR (2.4±1.5 vs. 2.6±1.4, p=0.7), intracoronary ACh 100μg provocation significantly increased CVR (2.1±2.2 vs. 0.8±0.7; p=0.001), and then attenuated CBF (77±54 vs. 188±129, p=0.001) in VSA group than in non-VSA group. Furthermore, although coronary flow reserve was identical between the groups (2.2±0.9 [VSA] vs. 2.4±0.9 [non-VSA], p=0.5), hMR was significantly augmented in VSA group (2.0±0.7 vs. 1.6±0.6, p=0.046). Also, there was significantly negative correlation between hMR and estimated glomerular filtration rate, which presumably reflect the integrity of renal MV bed (r=-0.522; p=0.0009). Conclusions: Compared with non-VSA pts, coronary and systemic MV function was impaired in pts with VSA. In vivo assessment using Combowire clarified dynamic entire coronary alteration during ACh provocation test, including coronary MV dysfunction, in pts with VSA.

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