Tag: endothelial dysfunction


Coronary Slow Flow Is Not Diagnostic of Microvascular Dysfunction in...

Guidelines recommend that coronary slow flow phenomenon (CSFP), defined as corrected thrombolysis in myocardial infarction frame count (CTFC) >27, can diagnose coronary microvascular dysfunction (CMD) in patients with angina and nonobstructed coronary arteries.

CSFP has also historically been regarded as a sign of coronary endothelial dysfunction (CED). We sought to validate the utility of CTFC, as a binary classifier of CSFP and as a continuous variable, to diagnose CMD and CED.

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Vasospastic Angina: A Contemporary Review of its Pathophysiology, Diagnosis and...

Nearly 40% of patients presenting to the catheter laboratory with angina have non-obstructed coronary arteries (ANOCA), an umbrella term that encompasses distinct pathophysiological entities, such as coronary artery spasm.

Coronary artery spasm leads to sudden reversible coronary flow attenuation, which clinically manifests as vasospastic angina (VSA). VSA is associated with poor quality of life and an increased risk of major adverse cardiac events. However, the pathophysiological mechanisms underlying this phenomenon are incompletely understood, which has resulted in limited therapeutic options for patients afflicted with this condition. The past decade has seen a surge in new research being conducted in the field of ANOCA and VSA.

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Pathophysiology of Coronary Microvascular Dysfunction

Ischemic heart disease (IHD) is commonly recognized as the consequence of coronary atherosclerosis and obstructive coronary artery disease (CAD). However, a significant number of patients may present angina or myocardial infarction even in the absence of any significant coronary artery stenosis and impairment of the coronary microcirculation has been increasingly implicated as a relevant cause of IHD.

The term “coronary microvascular dysfunction” (CMD) encompasses several pathogenic mechanisms resulting in functional and/or structural changes in the coronary microcirculation and determining angina and myocardial ischemia in patients with angina without obstructive CAD (“primary” microvascular angina), as well as in several other conditions, including obstructive CAD, cardiomyopathies, Takotsubo syndrome and heart failure, especially the phenotype with preserved ejection fraction.

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Coronary Artery Spasm: The Interplay Between Endothelial Dysfunction and Vascular...

Patients with angina pectoris, the cardinal symptom of myocardial ischaemia, yet without significant flow-limiting epicardial artery stenosis represent a diagnostic and therapeutic challenge. Coronary artery spasm (CAS) is an established cause for anginal chest pain in patients with angiographically unobstructed coronary arteries. CAS may occur at the epicardial level and/or in the microvasculature.

Although the underlying pathophysiological mechanisms of CAS are still largely unclear, endothelial dysfunction and vascular smooth muscle cell (VSMC) hyperreactivity seem to be involved as major players, although their contribution to induce CAS is still seen as controversial.

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Around The World

Real Patient Stories

Lynn’s story

I had my first spasm when I was just a young child and continued for almost 50 years with no diagnosis. I always assumed everybody had flushing feelings throughout their body, and hot flashes accompanied by chest pain.

It wasn’t until I was walking my dogs with my sister, one day, and we were going up a steep incline and I couldn’t keep up. I asked her if she felt chest pains when she walked up hills. She looked at me like I was crazy and told me: No!

I then realized something might be wrong with me.

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Dima’s story

March 3rd, 2021 was the day that changed everything. At 55, I had a busy counselling practice and a few other projects on the go. The pandemic was causing anxiety for many of my clients and in my private life. I had a lot of stress of my own: there were safety issues in the building where I lived, and I was looking for a new apartment. Despite this, I thought I was handling it well. I was fairly healthy, I walked daily, ate well, meditated and didn’t smoke or drink.

I started to experience heavy fatigue towards the end of 2020 but told myself it was normal considering all that was going on in the world.

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MaryAnn’s story

When I was 39, with zero risk factors for heart disease, I had all the classic symptoms associated with a heart attack. My doctors put me on three blood thinners to dissolve a clot in a minor artery seen in an angiogram. The next day, while the original clot had dissolved, I had a clot in a larger artery. Baffled, the cardiologists put in a stent. As they backed the scope out of the artery, it spasmed in another location.

At that time, I had a 4-year-old, an 8-year-old, and a 12-year-old. My husband traveled extensively for work. I asked myself two questions: 1) How do I feel about dying at age 39? 2) If I don’t die, how do I live?

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