Tag: endothelial dysfunction

Research

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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Research

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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Research

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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Research

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

Sandra’s story

My story began in January 2010, while sitting at a traffic light returning to the office. I was working as a home health physical therapist. I began having chest pain out of nowhere. I got to my office and my boss, an RN, asked me if I was OK. I told her about the chest pain. By then it was starting to progress down my left arm. She took my blood pressure, normally 98/68. It was 140/90. She called my husband and told him to meet me at the ER. I drove myself there. They ran the normal tests and diagnosed me with costochondritis. Pain meds made the symptoms go away. The pain came back six times in the next 6 months. I asked for a cardiologist referral, but was denied, due to my age (39), lack of family history, and being in shape.

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Sinéad’s story

My first episode caught me completely off guard on a Sunday morning in 2014. I was an active, healthy 35-year-old mother of 3. It felt like what I imagined having a heart attack would feel like. After a minute or two it stopped as suddenly as it had started and I got out of bed to start my day, I had experienced palpitations before and brushed it off as a once off.

I had about 8 more episodes before lunch time and made a deal with myself that if it continued, I would call an ambulance. I was a busy mum and didn’t want to be ‘dramatic’! It resolved by 2 p.m.

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Don’s story

I consider myself one of the lucky ones.

I was a runner, triathlete, skier, scuba diver, etc. before my problems got severe enough to seek medical help.

Most doctors took my health decline seriously from the start.

Later, it was not uncommon for doctors who were unaware of my athletic endeavours to assume my subsequent lack of fitness was the cause of my condition rather than the result.

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