Category: Research

Research

Functional coronary angiography for the assessment of the epicardial vessels...

Over the last decade, steady progress has been made in the ability to assess coronary stenosis relevance by merging computerised analyses of angiograms with fluid dynamic modelling.

The new field of functional coronary angiography (FCA) has attracted the attention of both clinical and interventional cardiologists as it anticipates a new era of facilitated physiological assessment of coronary artery disease, without the need for intracoronary instrumentation or vasodilator drug administration, and an increased adoption of ischaemia-driven revascularisation.

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Research

Coronary Microvascular Spasm: Clinical Presentation and Diagnosis

Professor Maseri pioneered the research and treatment of coronary vasomotion abnormalities represented by coronary vasospasm and coronary microvascular dysfunction (CMD).

These mechanisms can cause myocardial ischaemia even in the absence of obstructive coronary artery disease, and have been appreciated as an important aetiology and therapeutic target with major clinical implications in patients with ischaemia with non-obstructive coronary artery disease (INOCA). Coronary microvascular spasm is one of the key mechanisms responsible for myocardial ischaemia in patients with INOCA.

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Research

Design and rationale of the NetherLands registry of invasive Coronary...

Angina without angiographic evidence of obstructive coronary artery disease (ANOCA) is a highly prevalent condition with insufficient pathophysiological knowledge and lack of evidence-based medical therapies. This affects ANOCA patients prognosis, their healthcare utilization and quality of life.

In current guidelines, performing a coronary function test (CFT) is recommended to identify a specific vasomotor dysfunction endotype. The NetherLands registry of invasive Coronary vasomotor Function testing (NL-CFT) has been designed to collect data on ANOCA patients undergoing CFT in the Netherlands.

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Research

ANOCA/INOCA/MINOCA: Open artery ischemia

Ischemic heart disease continues to represent a major health threat for death, disability, and poor quality of life as it also consumes enormous health-related resources. For over a century, the major clinical phenotype was taken to be obstructive atherosclerosis involving the larger coronary arteries (e.g., coronary artery disease [CAD]). However, evolving evidence now indicates that nonobstructive CAD is the predominant phenotype.

Patients within this phenotype have been termed to have angina with no obstructive CAD (ANOCA), ischemia with no obstructive CAD (INOCA), or myocardial infarction with no obstructive coronary arteries (MINOCA). But as methods to assess cardiomyocyte injury evolve, these phenotypic distinctions have begun to merge, raising concern about their usefulness.

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Research

Phenotype-based management of coronary microvascular dysfunction

40-70% of patients undergoing invasive coronary angiography with signs and symptoms of ischemia are found to have no obstructive coronary artery disease (INOCA). When this heterogeneous group undergo coronary function testing, approximately two-thirds have demonstrable coronary microvascular dysfunction (CMD), which is independently associated with adverse prognosis.

There are four distinct phenotypes, or subgroups, each with unique pathophysiological mechanisms and responses to therapies. The clinical phenotypes are microvascular angina, vasospastic angina, mixed (microvascular and vasospastic), and non-cardiac symptoms (reclassification as non-INOCA). The Coronary Vasomotor Disorders International Study Group (COVADIS) have proposed standardized criteria for diagnosis.

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Research

Precision medicine versus standard of care for patients with myocardial...

Myocardial infarction with non-obstructive coronary arteries (MINOCA) represents about 6-8% of patients presenting with myocardial infarction (MI), and it is associated with a significant risk of mortality, rehospitalisation, and angina burden, with high associated socioeconomic costs.

It is important to note that multiple mechanisms may be responsible for MINOCA. However, to date, there are few prospective clinical trials on MINOCA and the treatment of these patients is still not defined, most likely because of the multiple underlying pathogenic mechanisms.

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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

Prognostic association of plasma NT-proBNP levels in patients with microvascular...

The aim of this study was to assess the prognostic association of plasma levels of N-terminal prohormone of brain natriuretic peptide (NT-proBNP) with clinical outcomes of patients with microvascular angina (MVA).

In this international prospective cohort study of MVA by the Coronary Vasomotor Disorders International Study (COVADIS) group, we examined the association between plasma NT-proBNP levels and the incidence of major adverse cardiovascular events (MACE), including cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, and hospitalization due to heart failure or unstable angina.

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Research

Air Pollution and Coronary Vasomotor Disorders in Patients With Myocardial...

Coronary vasomotor abnormalities are important causes of myocardial ischemia in patients with nonobstructive coronary artery disease (NOCAD). However, the role of air pollution in determining coronary vasomotor disorders has never been investigated.

We aimed to evaluate the association between long-term exposure to particulate matter 2.5 (PM2.5) and 10 (PM10), and coronary vasomotor disorders in NOCAD patients.

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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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Around The World

Real Patient Stories

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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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