Background: An association between atherosclerosis and coronary vasospasm has previously been suggested. However, to date, no conclusive data on the whole spectrum of these disorders have been published.
Aims: This study aimed to define specific morphological features of atherosclerosis in patients with angina and no obstructive coronary artery disease (ANOCA) due to coronary vasospasm.
The evaluation of stable chest pain suspected to be cardiac in nature has traditionally involved the use of a screening noninvasive investigation, with invasive selective coronary angiography being the benchmark investigation.
Moreover, if the noninvasive investigation implicates the presence of myocardial ischemia (ie, new ischemic electrocardiographic [ECG] changes, perfusion defect, or regional wall abnormality) and the invasive coronary angiogram shows no evidence of obstructive coronary artery disease (CAD), then the noninvasive investigation is considered a false positive and the patient receives a diagnosis of “noncardiac chest pain.”
In the absence of obstructive coronary stenoses, abnormality of noninvasive stress tests (NIT) in patients with chronic coronary syndromes may indicate myocardial ischemia of nonobstructive coronary arteries (INOCA). The differential prognosis of INOCA according to the presence of coronary microvascular dysfunction (CMD) and incremental prognostic value of CMD with intracoronary physiologic assessment on top of NIT information remains unknown.
In stable patients with nonobstructive coronary stenoses, a diagnosis of INOCA based only on abnormal NIT did not identify patients with higher risk of long‐term cardiovascular events. Incorporating intracoronary physiologic assessment to NIT information in patients with nonobstructive disease allowed identification of patient subgroups with up to 4‐fold difference in long‐term cardiovascular events.
Endothelial cell damage related to coronavirus disease 2019 (COVID-19) has been described in multiple vascular beds, and many survivors of COVID-19 report chest pain. This case series describes two previously healthy middle-aged individuals who survived COVID-19 and were subsequently found to have symptomatic coronary endothelial dysfunction months after initial infection.
The novel coronavirus 2019 and the associated coronavirus-related respiratory distress syndrome (SARS-CoV2) have caused a worldwide pandemic with over 100,000,000 people infected. Acute cardiovascular manifestations of coronavirus disease 2019 (COVID-19) include myocarditis, ST-elevation myocardial infarction, arrhythmias, vascular endothelial dysfunction, and coronary vasospasm.
Intracoronary provocation testing with acetylcholine (ACh) is crucial for the diagnosis of functional coronary alterations in patients with suspected myocardial ischaemia and non-obstructive coronary arteries.
Our intention was to assess the safety and predictive value for major adverse cardiovascular and cerebrovascular events (MACCE) in patients presenting with ischaemia with non-obstructive coronary arteries (INOCA) or with myocardial infarction with non-obstructive coronary arteries (MINOCA).
We prospectively enrolled consecutive INOCA or MINOCA patients undergoing intracoronary ACh provocation testing.
Nearly half of all patients with angina have non-obstructive coronary artery disease (ANOCA); this is an umbrella term comprising heterogeneous vascular disorders, each with disparate pathophysiology and prognosis. Approximately two-thirds of patients with ANOCA have coronary microvascular disease (CMD). CMD can be secondary to architectural changes within the microcirculation or secondary to vasomotor dysfunction.
An inability of the coronary vasculature to augment blood flow in response to heightened myocardial demand is defined as an impaired coronary flow reserve (CFR), which can be measured non-invasively, using imaging, or invasively during cardiac catheterisation. Impaired CFR is associated with myocardial ischaemia and adverse cardiovascular outcomes.
Coronary vasomotor dysfunction can be diagnosed in a large proportion of patients with angina in the presence of non-obstructive coronary artery disease (ANOCA) using comprehensive protocols for coronary vasomotor function testing (CFT). Although consensus on diagnostic criteria for endotypes of coronary vasomotor dysfunction has been published, consensus on a standardised study testing protocol is lacking.
In this review we provide an overview of the variations in CFT used and discuss the practical principles and pitfalls of CFT.
Coronary functional abnormalities are frequent causes of angina pectoris, particularly in patients with unobstructed coronary arteries. There is a spectrum of endotypes of functional coronary abnormalities with different mechanisms of pathology including enhanced vasoconstriction (i.e. coronary artery spasm) or impaired vasodilatation, such as impaired coronary flow reserve or increased microvascular resistance.
These vasomotor abnormalities can affect various compartments of the coronary circulation such as the epicardial conduit arteries and/or the coronary microcirculation. Unequivocal categorisation and nomenclature of the broad spectrum of disease endotypes is crucial both in clinical practice as well as in clinical trials.
Up to half of patients undergoing elective coronary angiography for the investigation of chest pain do not present with evidence of obstructive coronary artery disease. These patients are often discharged with a diagnosis of non-cardiac chest pain, yet many could have an ischaemic basis for their symptoms. This type of ischaemic chest pain in the absence of obstructive coronary artery disease is referred to as INOCA (ischaemia with non-obstructive coronary arteries).
This comprehensive review of INOCA management looks at why these patients require treatment, who requires treatment based on diagnostic evaluation, what clinical treatment targets should be considered, how to treat patients using a personalised medicine approach, when to initiate treatment, and where future research is progressing.
Intracoronary physiology testing has emerged as a valuable diagnostic approach in the management of patients with chronic coronary syndrome, circumventing limitations like inferring coronary function from anatomical assessment and low spatial resolution associated with angiography or non-invasive tests.
The value of hyperaemic translesional pressure ratios to estimate the functional relevance of coronary stenoses is supported by a wealth of prognostic data. The continuing drive to further simplify this approach led to the development of non-hyperaemic pressure-based indices. Recent attention has focussed on estimating physiology without even measuring coronary pressure.
Recognition of suspected ischaemia with no obstructive coronary artery disease – termed INOCA – has increased over the past decades, with a key contributor being microvascular angina. Patients with microvascular angina are at higher risk for major adverse cardiac events including MI, stroke, heart failure with preserved ejection fraction and death but to date there are no clear evidence-based guidelines for diagnosis and treatment.
Recently, the Coronary Vasomotion Disorders International Study Group proposed standardised criteria for diagnosis of microvascular angina using invasive and non-invasive approaches. The management strategy remains empirical, largely due to the lack of high-level evidence-based guidelines and clinical trials. In this review, the authors will illustrate the updated approach to the diagnosis of microvascular angina and address evidence-based pharmacological and non-pharmacological treatments for patients with the condition.
Cardiovascular disease (CVD) remains the leading cause of death in women globally. Younger women (<55 years of age) who experience MI are less likely to receive guideline-directed medical therapy (GDMT), have a greater likelihood of readmission and have higher rates of mortality than similarly aged men. Women have been under-represented in CVD clinical trials, which limits the generalisability of results into practice. Available evidence indicates that women derive a similar benefit as men from secondary prevention pharmacological therapies, such as statins, ezetimibe, proprotein convertase subtilisin/kexin type 9 inhibitors, icosapent ethyl, antiplatelet therapy, sodium–glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists. Women are less likely to be enrolled in cardiac rehabilitation programs than men.
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.
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?
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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