scholarly journals Close Relationship Between Sympathetic Activation and Coronary Microvascular Dysfunction During Acute Hyperglycemia in Subjects With Atherosclerotic Risk Factors

2007 ◽  
Vol 71 (2) ◽  
pp. 202-206 ◽  
Author(s):  
Yasuyoshi Takei ◽  
Hirofumi Tomiyama ◽  
Nobuhiro Tanaka ◽  
Akira Yamashina
Keyword(s):  
Risk Factors ◽  
Microvascular Dysfunction ◽  
Coronary Microvascular Dysfunction ◽  
Sympathetic Activation ◽  
Acute Hyperglycemia ◽  
Close Relationship ◽  
Atherosclerotic Risk Factors

Relation between cardiovascular risk factors and coronary microvascular dysfunction in cardiac syndrome X

2011 ◽  
Vol 12 (5) ◽  
pp. 322-327 ◽  
Author(s):  
Alfonso Sestito ◽  
Gaetano A Lanza ◽  
Antonio Di Monaco ◽  
Priscilla Lamendola ◽  
Giulia Careri ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Microvascular Dysfunction ◽  
Syndrome X ◽  
Coronary Microvascular Dysfunction ◽  
Cardiac Syndrome X ◽  
Cardiac Syndrome

scholarly journals Coronary Microvascular Dysfunction　― Epidemiology, Pathogenesis, Prognosis, Diagnosis, Risk Factors and Therapy ―

2017 ◽  
Vol 81 (1) ◽  
pp. 3-11 ◽  
Author(s):  
Cheng Chen ◽  
Janet Wei ◽  
Ahmed AlBadri ◽  
Parham Zarrini ◽  
C. Noel Bairey Merz
Keyword(s):  
Risk Factors ◽  
Microvascular Dysfunction ◽  
Coronary Microvascular Dysfunction

Abstract 5636: Major Depression is Associated with Decreased Coronary Flow Reserve Detected by Positron Emission Tomography

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Viola Vaccarino ◽  
J D Bremner ◽  
John Votaw ◽  
Tracy Faber ◽  
Emir Veledar ◽  
...  
Keyword(s):  
Risk Factors ◽  
Positron Emission Tomography ◽  
Myocardial Perfusion ◽  
Coronary Flow Reserve ◽  
Coronary Flow ◽  
Microvascular Dysfunction ◽  
Emission Tomography ◽  
Coronary Microvascular Dysfunction ◽  
Flow Reserve ◽  
Positron Emission

Introduction. Major depressive disorder (MDD) is associated with coronary heart disease, but the underlying mechanisms are unclear. Coronary flow reserve (CFR) in response to adenosine is an index of coronary microvascular dysfunction which predisposes to myocardial ischemia. We examined the relationship between MDD and CFR in a genetically informative sample. Methods. We studied 141 twin pairs drawn from the Vietnam Era Twin Registry who were born between 1946 and 1956 (mean age 54). For all twins, a lifetime history of MDD was determined with the Structured Clinical Interview for Psychiatry Disorders; 53 pairs were discordant for MDD and 88 pairs were free of MDD. Standard cardiovascular risk factors were obtained by interview and examination. We performed myocardial perfusion imaging and blood flow quantitation with [13N] ammonia positron emission tomography at rest and after adenosine stress. A perfusion defect score summed the number and severity of defects across 20 myocardial regions. CFR was measured as the ratio of maximum flow to baseline flow at rest. Mixed-effect and GEE models were used to conduct matched-pair analyses. Results. There was no difference in the distribution of abnormal scans, in summed rest or stress defect scores, and in heart rate/blood pressure responses to adenosine between twins with and without MDD. Among the DZ twin pairs discordant for MDD, the mean CFR was lower in twins with MDD than their brothers without MDD (2.36 ± 0.66 vs 2.75 ± 0.90; p=0.03); no significant difference in mean CFR was found in MZ discordant pairs (2.90±0.78 vs 2.64±0.64, p=0.13). The zygosity by MDD interaction was significant (p=0.01). Results did not change substantially after adjusting for cardiovascular disease risk factors and antidepressant use (adjusted interaction p=0.007). There were no differences in myocardial perfusion comparing twins in discordant pairs with twins in healthy pairs. Conclusions. MDD is associated with lower CFR in spite of no differences in visible perfusion defects, suggesting microvascular dysfunction. This association is largely due to shared genetic liability between depression and CFR, suggesting a common underlying pathophysiological process linking depression and coronary microvascular dysfunction. This research has received full or partial funding support from the American Heart Association, AHA National Center.

Coronary microvascular dysfunction is not associated with a history of reproductive risk factors in women with angina pectoris—An iPOWER substudy

Maturitas ◽  
2018 ◽  
Vol 107 ◽  
pp. 110-115 ◽  
Author(s):  
Hannah Elena Suhrs ◽  
Anna Meta Kristensen ◽  
Anna Bay Rask ◽  
Marie Mide Michelsen ◽  
Daria Frestad ◽  
...  
Keyword(s):  
Risk Factors ◽  
Angina Pectoris ◽  
Microvascular Dysfunction ◽  
Coronary Microvascular Dysfunction ◽  
Reproductive Risk ◽  
History Of ◽  
Reproductive Risk Factors

Abstract 2948: Evidence of Coronary Microvascular Dysfunction in patients with Systemic Inflammatory Diseases

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Alejandro Recio-Mayoral ◽  
M B Rubens ◽  
J C Kaski ◽  
O Harari ◽  
P G Camici
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Lupus Erythematosus ◽  
Inflammatory Diseases ◽  
Microvascular Dysfunction ◽  
Coronary Microvascular Dysfunction ◽  
Ecg Changes ◽  
Flow Reserve ◽  
Positron Emission

Purpose: Accelerated coronary disease is a leading cause of morbidity and mortality in patients (pts) suffering from immune-mediated inflammatory diseases (IMID), such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). We tested the hypothesis that inflammation, in the absence of conventional cardiovascular risk factors, could result in coronary microvascular dysfunction (CMD) which is known to precede atherosclerosis in large vessels in pts with cardiovascular risk factors. Methods: Myocardial blood flow (MBF, ml/min/g) was measured using positron emission tomography at rest and during i.v. adenosine (140 μg/Kg/min) in 8 SLE and 10 RA pts aged 47 ± 8 years without conventional cardiovascular risk factors and in 18 age and gender matched controls. In pts multislice (64 slices) CT coronary angiography was performed to exclude coronary stenoses. Results: Mean disease duration was 18 ± 11 and 14 ± 6 years in RA and SLE respectively. There was no difference in resting MBF between pts and controls (1.27 ± 0.25 vs 1.11 ± 0.23; p=0.06). However, adenosine MBF was diffusely reduced in pts compared with controls (2.72 ± 0.84 vs 4.20 ± 0.75; p<0.0001) (Figure ). Coronary flow reserve (CFR; adenosine/resting MBF) was significantly reduced in pts (2.24 ± 0.74) compared with controls (4.00 ± 0.83; p<0.0001). Six pts showed ECG changes during adenosine stress and had a more severe reduction in CFR (1.73 ± 0.88) compared with those without ECG changes (2.49 ± 0.54; p<0.006). Conclusions: Patients with IMID and without conventional cardiovascular risk factors have evidence of CMD which can result in reductions of CFR severe enough to cause myocardial ischemia.

scholarly journals Plasma Lipidomic Patterns in Patients with Symptomatic Coronary Microvascular Dysfunction

Metabolites ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 648
Author(s):  
Jonathan R. Lindner ◽  
Brian P. Davidson ◽  
Zifeng Song ◽  
Claudia S. Maier ◽  
Jessica Minnier ◽  
...  
Keyword(s):  
Risk Factors ◽  
High Resolution Mass Spectrometry ◽  
Contrast Echocardiography ◽  
Microvascular Dysfunction ◽  
Carbon Chain ◽  
Elderly Subjects ◽  
Coronary Microvascular Dysfunction ◽  
Metabolic Demand ◽  
Long Chain Fatty Acid ◽  
Artery Disease

Coronary microvascular dysfunction (MVD) is a syndrome of abnormal regulation of vascular tone, particularly during increased metabolic demand. While there are several risk factors for MVD, some of which are similar to those for coronary artery disease (CAD), the cause of MVD is not understood. We hypothesized that MVD in symptomatic non-elderly subjects would be characterized by specific lipidomic profiles. Subjects (n = 20) aged 35–60 years and referred for computed tomography coronary angiography (CTA) for chest pain but who lacked obstructive CAD (>50% stenosis), underwent quantitative regadenoson stress-rest myocardial contrast echocardiography (MCE) perfusion imaging for MVD assessment. The presence of MVD defined by kinetic analysis of MCE data was correlated with lipidomic profiles in plasma measured by liquid chromatography and high-resolution mass spectrometry. Nine of twenty subjects had evidence of MVD, defined by reduced hyperemic perfusion versus other subjects (beta-value 1.62 ± 0.44 vs. 2.63 ± 0.99 s−1, p = 0.009). Neither the presence of high-risk but non-obstructive CAD on CTA, nor CAD risk factors were different for those with versus without MVD. Lipidomic analysis revealed that patients with MVD had lower concentrations of long-carbon chain triacylglycerols and diacylglycerols, and higher concentrations of short-chain triacylglycerols. The diacylglycerol containing stearic and linoleic acid classified all participants correctly. We conclude that specific lipidomic plasma profiles occur in MVD involving saturated long-chain fatty acid-containing acylglycerols that are distinctly different from those in non-obstructive CAD. These patterns could be used to better characterize the pathobiology and potential treatments for this condition.

scholarly journals Role of Inflammation in Coronary Epicardial and Microvascular Dysfunction

2021 ◽  
Vol 16 ◽  
Author(s):  
Shigeo Godo ◽  
Jun Takahashi ◽  
Satoshi Yasuda ◽  
Hiroaki Shimokawa
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Current Knowledge ◽  
Vascular Inflammation ◽  
Microvascular Dysfunction ◽  
Coronary Microvascular Dysfunction ◽  
Low Grade ◽  
Coronary Vasomotion ◽  
Close Relationship ◽  
Underlying Mechanisms

There is accumulating evidence highlighting a close relationship between inflammation and coronary microvascular dysfunction (CMD) in various experimental and clinical settings, with major clinical implications. Chronic low-grade vascular inflammation plays important roles in the underlying mechanisms behind CMD, especially in patients with coronary artery disease, obesity, heart failure with preserved ejection fraction and chronic inflammatory rheumatoid diseases. The central mechanisms of coronary vasomotion abnormalities comprise enhanced coronary vasoconstrictor reactivity, reduced endothelium-dependent and -independent coronary vasodilator capacity and increased coronary microvascular resistance, where inflammatory mediators and responses are substantially involved. How to modulate CMD to improve clinical outcomes of patients with the disorder and whether CMD management by targeting inflammatory responses can benefit patients remain challenging questions in need of further research. This review provides a concise overview of the current knowledge of the involvement of inflammation in the pathophysiology and molecular mechanisms of CMD from bench to bedside.

scholarly journals Experimental animal models of coronary microvascular dysfunction

2020 ◽  
Vol 116 (4) ◽  
pp. 756-770 ◽  
Author(s):  
Oana Sorop ◽  
Jens van de Wouw ◽  
Selena Chandler ◽  
Vahagn Ohanyan ◽  
Johnathan D Tune ◽  
...  
Keyword(s):  
Risk Factors ◽  
Animal Models ◽  
Obstructive Coronary Artery Disease ◽  
Subsequent Development ◽  
Microvascular Dysfunction ◽  
Transgenic Animal ◽  
Experimental Models ◽  
Therapeutic Interventions ◽  
Coronary Microvascular Dysfunction ◽  
Novel Therapeutic

Abstract Coronary microvascular dysfunction (CMD) is commonly present in patients with metabolic derangements and is increasingly recognized as an important contributor to myocardial ischaemia, both in the presence and absence of epicardial coronary atherosclerosis. The latter condition is termed ‘ischaemia and no obstructive coronary artery disease’ (INOCA). Notwithstanding the high prevalence of INOCA, effective treatment remains elusive. Although to date there is no animal model for INOCA, animal models of CMD, one of the hallmarks of INOCA, offer excellent test models for enhancing our understanding of the pathophysiology of CMD and for investigating novel therapies. This article presents an overview of currently available experimental models of CMD—with an emphasis on metabolic derangements as risk factors—in dogs, swine, rabbits, rats, and mice. In all available animal models, metabolic derangements are most often induced by a high-fat diet (HFD) and/or diabetes mellitus via injection of alloxan or streptozotocin, but there is also a wide variety of spontaneous as well as transgenic animal models which develop metabolic derangements. Depending on the number, severity, and duration of exposure to risk factors—all these animal models show perturbations in coronary microvascular (endothelial) function and structure, similar to what has been observed in patients with INOCA and comorbid conditions. The use of these animal models will be instrumental in identifying novel therapeutic targets and for the subsequent development and testing of novel therapeutic interventions to combat ischaemic heart disease, the number one cause of death worldwide.

Popliteal entrapment syndrome and age

VASA ◽  
2012 ◽  
Vol 41 (4) ◽  
pp. 262-268 ◽  
Author(s):  
Schweizer ◽  
Hügli ◽  
Koella ◽  
Jeanneret
Keyword(s):  
Risk Factors ◽  
Leg Pain ◽  
Walking Distance ◽  
Therapeutic Approaches ◽  
Long Distance ◽  
Entrapment Syndrome ◽  
Long Distance Running ◽  
Popliteal Entrapment ◽  
Popliteal Entrapment Syndrome ◽  
Atherosclerotic Risk Factors

On the occasion of diagnosing a popliteal entrapment syndrome in a 59-year old man with no cardiovascular risk factors, who developed acute ischemic leg pain during long distance running, we give an overview on this entity with emphasis on patients’age. The different types of the popliteal artery compression syndrome are summarized. The diagnostic and therapeutic approaches are discussed. The most important clinical sign of a popliteal entrapment syndrome is the lack of atherosclerotic risk factors in patients with limited walking distance. Not only in young athletes but also in patients more than 50 years old the popliteal entrapment syndrome has to be taken into account.

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