COVID-19-associated spontaneous coronary artery dissection

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Main article: COVID-19

For COVID-19 frequently asked inpatient questions, click here

For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ayesha Javid, MBBS[2] Rinky Agnes Botleroo, M.B.B.S.

Overview

Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is caused by novel coronavirus disease 2019 virus (COVID‐19).It has infected over 1.5 million patients worldwide with cardiac manifestations and injury in up to 20–28% of patients.Spontaneous coronary artery dissection (SCAD) is a non-iatrogenic non-traumatic separation of the coronary arterial wall. It could be either atherosclerotic or non-atherosclerotic.

Historical Perspective

• COVID-19 was first reported in Wuhan, Hubei Province,China in December 2019.
• The World Health Organization declared the COVID-19 outbreak a pandemic on March 12, 2020.
• On June 22, 2020, the first case of COVID-19 with spontaneous coronary artery dissection was reported.

Classification

• Based on origin COVID-19 associated spontaneous coronary artery dissection can be of two types:
  • Atherosclerotic (A-SCAD)
  • Non-atherosclerotic (NA-SCAD)

Pathophysiology

• SCAD can be secondary to an atherosclerotic (A-SCAD) or non-atherosclerotic (NA-SCAD) lesion.
• Lessons from the previous coronavirus and influenza epidemics suggest that these viral infections can trigger acute coronary syndrome primarily owing to a combination of a significant systemic inflammatory response plus localized vascular inflammation at the arterial plaque level.

Atherosclerotic-Spontaneous Coronary Artery Dissection (A-SCAD) :

• While the exact mechanism of cardiac injury in this population is unknown, the proposed etiology is thought that as a result of the infection there is changes in myocardial demand leading to an ischemic cascade and increased inflammatory markers that predispose patients to plaque instability and subsequent rupture.

• Coronary artery dissection may be related to intraplaque hemorrhage resulting in an intra-adventitial hematoma,which can spread longitudinally along the coronary artery, dissecting the tunicae.
• In COVID-19 patients due to high inflammatory load, a localized inflammation of the coronary adventitia and periadventitial fat can occur. This can lead to the development of sudden coronary artery dissection in a susceptible patient with underlying cardiovascular disease.
  

Non-Atherosclerotic-Spontaneous Coronary Artery Dissection (NA-SCAD):

• Contemporary usage of the term ‘SCAD’ is typically synonymous with NA-SCAD. It can result in extensive dissection lengths, especially in the presence of arterial fragility from predisposing arteriopathies.
• NA-SCAD can develop in any layer (intima , media, or adventitia) of the coronary artery wall. However, the initiation and the pattern of dissection in NA-SCAD is different from the pattern observed in patients with pre-existing atherosclerosis.
• At present the pathophysiology of non-atherosclerotic spontaneous coronary artery dissection (NA-SCAD) continues to be poorly understood due to the rarity of this condition and its heterogeneous pathology. Although intimal tear or bleeding of vasa vasorum with intramedial hemorrhage seems to be most probable reasons, the exact underlying mechanism is still unknown.

To read more about the pathophysiology of Spontaneous Coronary Artery Dissection, Click here.

Causes

• COVID‐19 associated spontaneous coronary artery dissection is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS‐CoV‐2).
• For other causes of spontaneous coronary artery dissection, Click here.

Differentiating COVID-19-associated spontaneous coronary artery dissection from other Diseases

Differential Diagnosis	Similarities	Differences
Athersclerotic Acute Coronary Syndrome	Clinical presentation: Sudden chest pain, Shortness of breath, Nausea,Vomiting Acute and Chronic recanalised atheroscheloric thrombus may mimic type 1 double lumen SCAD	Male predominance Older patients than SCAD High prevalance of cardiovascular risk factor No association with fibromuscular dysplasia Less coronary tortuosity PCR assay for COVID-19 negative
Takotsubo Cardiomyopathy	Clinical presentation: Sudden chest pain, Shortness of breath, Nausea,Vomiting Female sex predominance Frequently preceeded by stress(psychological/emotional) Predominance of Left Anterior Descending Artery	Older patients than SCAD No diagnostic findings on coronary angiogram PCR assay for COVID-19 negative
Coronary Embolism	Late angiographic healing Predominance of distal coronary segments	Presence of high risk conditions for systemic embolism for example: Atrial Fibrilation,Prosthetic heart valves,Dilated Cardiomyopathy with apical thrombus,Infective endocarditis PCR assay for COVID-19 negative
Coronary Spasm	Sometimes multifocal/multivessel involvement	Male sex predominance Difference in clinical presentation( typically angina at rest,during the night) PCR assay for COVID-19 negative

Epidemiology and Demographics

• Huang et al reported that 12% of patients with COVID-19 were diagnosed to have acute myocardial injury. According other recent data, among 138 hospitalized patients with COVID-19, 16.7% had arrhythmias and 7.2% had acute myocardial injury.
• A 55-year-old man with a medical history of peripheral artery disease also was diagnosed with COVID-19 associated SCAD
• A 70-year-old man with COVID-19 associated SCAD was reported in March 2020.

• A 48-year-old woman with a past medical history of migraine and hyperlipidemia also reported having COVID-19 associated SCAD

Risk Factors

• Patients with COVID-19 infection who have underlying Cardiovascular disease are more likely to develop SCAD and more severe adverse outcomes when myocardial injury occurs after COVID-19 infection and face higher risk of death,
• There is often an associated underlying predisposing arteriopathy, which may be compounded by a precipitating stressor, culminating in the phenotypic expression of SCAD
• Predisposing Factors:
  • Fibromuscular dysplasia
  • Pregnancy
  • Recurrent pregnancies: multiparity or multigravida
  • Connective tissue disorder: Marfan syndrome, Loeys-Dietz syndrome, Ehler-Danlos syndrome type 4, cystic medial necrosis, alpha-1 antitrypsin deficiency, polycystic kidney disease
  • Systemic inflammatory disease: systemic lupus erythematosus, Crohn’s disease, ulcerative colitis, polyarteritis nodosa, sarcoidosis, Churg-Strauss syndrome, Wegener’s granulomatosis, rheumatoid arthritis, Kawasaki, giant cell arteritis, celiac disease
  • Hormonal therapy: oral contraceptive, estrogen, progesterone, beta-HCG, testosterone, corticosteroids
  • Coronary artery spasm
  • Idiopathic
• Precipitating stressors:
  • Strenous exercises (isometric or aerobic activities)
  • Intense emotional stress
  • Labor and delivery
  • Intense Valsalva-type activities (e.g., retching, vomiting, bowel movement, coughing)
  • Recreational drugs (e.g., cocaine, amphetamines, metamphetamines)
  • Intense hormonal therapy (e.g., beta-HCG injections, corticosteroids injections)

Screening

Evaluation of patients presenting to the inpatient and outpatient settings during this global pandemic with cardiac chief complaints requires a thorough history and examination to evaluate for potential infection with SARS‐CoV‐2. The virus should be on the differential for all clinicians as a possible cause of cardiopulmonary complaints. Understanding the range of cardiac manifestations and how they can affect patients can help clinicians to further care for patients with potential COVID‐19 infection.

Natural History, Complications, and Prognosis

Prognosis

Patients with COVID-19 infection who have underlying Cardiovascular disease are more likely to develop SCAD and more severe adverse outcomes when myocardial injury occurs after COVID-19 infection and face higher risk of death.Patients with prior cardiovascular injury have a fourfold increased risk of mortality compared to those without cardiovascular disease.

Diagnosis

History and Symptoms

SCAD can present as acute coronary syndrome and NSTEMI. The symptoms include:

• Sudden onset of retrosternal pain chest pain which remains persistent in a COVID-19 seropositive patient or in a patient with recent cough and dyspnea raises suspicion of SCAD.
• The chest pain can radiate to the left arm.
• It can be associated with the following symptoms:
  • Difficulty breathing
  • Loss of consciousness
  • Nausea and vomiting
  • Diaphoresis

• Here is a table presenting symptoms of the reported cases:
  

Patient	Symptoms	Past medical history and risk factors	Laboratory findings	Treatment
55 year old, male ,admitted due to cough and febrile dyspnea with suspected COVID-19.	48 hrs after admission had chest pain	Peripheral artery disease	EKG: Inverted T waves in the inferior leads Troponin I was elevated {Hs-TnI was at 355 ng/l, then 570 ng/l 3 h later (normal values <7 ng/l)} Transthoracic echocardiography:Left ventricular ejection fraction 60% without wall motion abnormalities, no diastolic dysfunction, and a mild mitral regurgitation Coronary angiogram : Chronic total occlusion of the posterior descending artery with epicardial collateral from the left anterior descending artery. In the mid-right coronary artery, a spontaneous dissecting coronary hematoma was observed with an intimal tear. Optical coherence tomography (OCT): spontaneous dissecting coronary hematoma with an intimal rupture of right coronary artery	Aspirin, Statins, and Beta-blockers. Subsequent control of coronary angiogram was planned.
70-year-old, male	Severe , persistent chest pain ( 8/10), which started 3 hrs before admission	Smoking, Hypertension, and Type 2 diabetes, H/O percutaneous coronary intervention (PCI) with implantation of a drug-eluting stent (DES)	EKG:new ST-T abnormalities in the precordial leads ST-T abnormalities in the precordial leads. Echocardiogram: Left ventricular ejection fraction 40–45% with akinesia in the LCx territory (old) and a severe hypokinesis in the left anterior ascending (LAD) territory. Coronary angiogram: moderate in-stent restenosis on LCx-OM and a moderate right coronary artery (RCA) stenosis	Heparin, Sublingual nitroglycerin, and Clopidogrel Angiogram was performed
48‐year‐old, female	History of severe chest pain that awoke her from sleep,9/10,severe,retrosternal tightness with radiation to neck and bilateral arms.	Migraine and Hyperlipidemia	Initial troponin I <0.01 with subsequent troponin I 0.5 ng/ml (reference range <0.80 ng/ml) Electrocardiogram: No acute ST changes or signs of ischemia Transthoracic echocardiogram : Left ventricular ejection fraction 45–50% and akinesis of the distal anteroseptal and apical segments Computed tomography coronary angiogram: LAD artery showed dissection from the mid‐to‐distal LAD	Aspirin, Sublingual nitroglycerin

Laboratory Findings

• Elevated serum troponin level.
• Increased high-sensitivity cardiac troponin T-test (hs-cTnT).
• Increased D-dimer.
• Blood count is usually in the normal range.
• Inflammatory markers are usually in the normal range.

ECG

• New ST-T abnormalities in the precordial leads which are not present earlier.
• Inverted T waves in the inferior leads.

Coronary angiography

• Invasive coronary angiography is the "gold standard" used for the diagnosis of SCAD.

Echocardiogram

• Left ventricular dysfunction with decreased ejection fraction is seen.
• Akinesia or hypokinesia is seen in the affected territory of the heart.

Intravascular ultrasound (IVUS) and optical coherence tomography (OCT)

• These imaging modalities show detailed morphology about the intramural lesion in situations when angiographic images are not clear. IVUS is important in the followup of the treatment of SCAD patients.
• OCT is superior for visualizing intimal tears, intraluminal thrombi, false lumens, and intramural hematoma, but it is limited by optical penetration and shadowing, and may not depict the entire depth of the Intramural hematoma.OCT is preferred for imaging SCAD due to its superiority and ease in visualizing intramural hematoma , intimal disruption, and double lumens.

Treatment

Medical management

• Antiplatelet therapy:The role of antiplatelet therapy for SCAD is unknown, but on the basis of the totality of evidence for aspirin in ACS and secondary prevention, together with its low side effect profile, aspirin appears reasonable to use for acute and long-term SCAD management. Clopidogrel for acute management of SCAD patients not treated with stents is of uncertain benefit.
• Statins::The use of statins for SCAD is controversial.The bulk of data for ACS demonstrates significant benefit with lipid lowering, and statins are routinely recommended post-MI. Because of the uncertainty and the general lack of atherosclerosis in SCAD patients, statins tend to only be administered to patients with pre-existing dyslipidemia.
• Beta-blockers: Beta-blocker is associated with decreased recurrence of SCAD..There is a general agreement that beta blockers take the most important place in the medical management of SCAD patients. These agents may improve the outcomes of SCAD patients with reducing vascular wall shear stress likewise in patients with aortic dissection.Furthermore, beta blockers should be used in these group of patients in order to reduce complications of myocardial infarction.

Percutaneous coronary artery intervention (PCI)

Conservative management should be first choice if emergent revascularization is not necessary.

To read more about PCI in Spontaneous Coronary Artery Dissection, Click here.

Surgery

Coronary Artery Bypass Graft (CABG)

Coronary Artery Bypass Graft (CABG) should be considered for patients with left main dissections, extensive dissections involving proximal arteries, or in patients in whom PCI failed or who are not anatomically suitable for PCI.

Prevention

• Limiting transmission of the SARS-CoV2 virus while protecting patients and members of healthcare team is a prime goal and cardiac catheterization laboratory protocols must be rapidly evolved to maintain high‐quality and safe cardiovascular care amidst the current pandemic.
• COVID‐19 testing prior to catheterization procedures where feasible
• Adequate PPE to protect team members in COVID‐19 unknown or pending cases to reduce the risk of unplanned aerosol producing procedure such as intubation or CPR.