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: Rinky Agnes Botleroo, M.B.B.S. Ayesha Javid, MBBS[2]

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

• The exact pathogenesis of spontaneous coronary artery dissection in covid-19 patients is not fully understood.
• It is thought that SCAD in covid-19 patients is the result of either Intense inflammation and endothelial dysfunction causing sympathetic overreactivity leading to intimal dissection.
• High dose of corticosteroid therapy may induce spontaneous rupture of injured arterial wall.
• Covid-19 may causes activation and infiltration of T cells in coronary adventitia and periadventitial fat leading to release of cytokines and protease and dissection of injured wall.
• Covid-19 may enhance angiogenesis and proliferation of vasavasarum.
• Rupture of fragiled vasavasarum is the cause of intramural hematoma.
• Transition of inflammatory cell via vasavasarum to the medial and adventitial layers of the vessels may lead to rupture of vasavasarum.
• Covid-19 may attach to ACE receptors on endothelial and smooth muscle of coronary artery leading to inflammation in the muscle wall, massive death of endotheliocytes, vascular tone impairment, hemostatic impairment, and vulnerability of vessels wall to dissection.

• SCAD can be secondary to an atherosclerotic (A-SCAD) or non-atherosclerotic (NA-SCAD) lesion in origin.
• 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 that as a result of the infection there are 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 the most probable reason, the exact underlying mechanism is still unknown.

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

Causes

Common causes of covid-19-associated with spomtaneous coronary artery dissection include:

• Inflammation
• sympathetic overreactivity
• Use of corticosteroids
• Underlying coronary artery disease

  For other causes of spontaneous coronary artery dissection, Click here.

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

• To view the differential diagnosis of COVID-19, click here.
  
• To view a differential diagnosis on the other causes of chest pain, click here.

Epidemiology and Demographics

• The prevalence of spontaneous coronary artery dissection in covid-19 is not determined yet. However, among nine reported cases in literatur , 22.3% were women and 77.7% were men.

Age

• the range of age of reported cases of spontaneous coronary artery dissection associated covid-19 in literature were between 35-70 years old.

Gender

• Women are more commonly affected with Spontaneous coronary artery dissection than men. However, six of the nine patients with covid-19 associated spontaneous coronary artery dissection were men.

Race

• There is no racial predilection for spontaneous coronary artery dissection associated with covid-19.

Risk Factors

• Among nine reported cases of covid-19 associated SCAD there were not any previous risk factors of SCAD.
• Conventionakl risk factors of spontaneous coronary artery dissection include:
  • 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
  • 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 require 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

• The majority of covid-19 patients with spontaneous coronary artery dissection are diagnosed with myocardial infarction.
• Early clinical features include STEMI, NSTEMI.
• If left untreated, covid-19 patients with SCAD may progress to develop hemodynamic instability, ongoing ischemia, malignant arrhythmia.
• High risk angiographic features of coronary artery include:

  Impaired coronary flow

  Multivessles proximal dissections

  Left main lesion

  Ostial LAD lesion

• Prognosis is dependent on the anatomical extension of dissection, and survival rate of all nine reported cases in literature were 100%.

Diagnosis

History and Symptoms

SCAD can present as acute coronary syndrome and STEMI. 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

  Cough can be the perscipitant factor in the development of SCAD in covid-19 patients. (10.1097/MCA.0000000000000991)

• Clinical characteristics of patients with covid-19 related spontaneous coronary artery dissection:
  

Age, sex	Cardiovascular history	Symptoms	Predisposing factors	Timing according to covid-19 infection	Concomitant covid-19 complications	Covid-19 severity	Diagnosis	Vessle	Treatment	Outcome
45 years, female	None	Anosmia, hypogeusia, chest pain	Not reported	8 weeks	None	Mild	STEMI	LAD	Conservative, dual antiplatelet, betablocker, ACE inhibitor	Survived
40 years, male	None	Fever, cough	Not reported	7 days after ECMO	Cardiogenic shock, severe respiratory distress syndrome, cardiac thrombosis	Severe lung infiltration	NSTEMI	LAD	Conservative	Survived
48 years, female	Hyperlipidemia	Chest pain	Not reported	COVID-19 PCR was tested after SCAD	Polymorphic ventricular tachycardia	Mild	STEMI	LAD	Conservative, dual antiplatelet, betablocker, amiodarone	Survived
55 years, male	Peripheral arterial disease	Fever, cough, chest pain, dyspnea	Not reported	48 hours after obtained test	None	Moderate, crazy pavy patten in lung	NSTEMI	RCA	Conservative, ASA, statin, betablocker	Survived
70 years, male	Smoker, hypertension, diabetes mellitus	Fever, chest pain	Not reported	Positive covid-19 test one day after angiography	None	Mild	NSTEMI	LAD	PCI, ASA, statin, betablocker, clopidogrel, metformine, pantoprazole	Survived
39 years, male	None	Fever, cough, myalgia, chest pain, dyspnea	Not reported	18 days after [[covid-19]	None	Severe, respiratory failure leading to intubation	STEMI	LAD, LCX	Conservative, dual antiplatelet	Survived
51 years, female	Hypertension, smoker	Fever, cough, dyspnea	Not reported	3 days	None	Mild	NSTEMI	LAD	Conservative, dual antiplatelet, anticoagulant, statin	Survived
35 years, male	Obese, smoker	Weakness, fever, nasal congestion, anosmia, dry cough, chest congestion	Autoimmune disease were ruled out	18 days	None	Mild	STEMI	RCA, Ramus intermedius	RCA conservative treatment, dual antiplatelet, anticoagulant, statin	Survived

Patient	Symptoms	Past medical history and risk factors	Laboratory/Imagings findings	Treatment
55 years old, male admitted due to Fever, Cough Shortness of breath with suspected COVID-19.	Developed chest pain 48 hrs after coming to the hospital	Peripheral artery disease	EKG: Inferior leads show Inverted T waves. Elevated Troponin I from 355 ng/l --->70 ng/l 3 h later (Normal values <7 ng/l)) Transthoracic echocardiography Left ventricular ejection fraction :60% No abnormalities in wall motion. Absence of diastolic dysfunction Presence of mild mitral regurgitation Coronary angiogram : Posterior descending artery is occluded Presence of epicardial collateral from the left anterior descending artery Intimal tear is present in the mid-right coronary artery with a spontaneous dissecting coronary hematoma Optical coherence tomography (OCT): Intimal rupture of right coronary artery Spontaneous dissecting coronary hematoma	Aspirin, Statins, and Beta-blockers. Coronary angiogram was planned.
70-year-old, male	Severe, persistent chest pain ( 8/10), which started 3 hrs before admission	Smoking Hypertension Type 2 diabetes History of percutaneous coronary intervention (PCI) with implantation of a drug-eluting stent (DES)	EKG: precordial leads shows new ST-T abnormalities that were not present previously. ST-T abnormalities in the precordial leads. Echocardiogram: Left ventricular ejection fraction : 40–45% Old akinesia in the left circumflex artery territory Severe hypokinesis in the left anterior ascending (LAD) Coronary angiogram: Moderate in-stent restenosis present on left circumflex artery-OM Right coronary artery (RCA) is stenosed.	Heparin, Sublingual nitroglycerin, and Clopidogrel Angiogram was performed
48‐year‐old, female History of severe chest pain that awoke her from sleep	Severe retrosternal chest pain,9/10, pain radiates to the neck, and both arms.	Migraine Hyperlipidemia	Elevated Troponin I from <0.01 to 0.5 ng/ml (Normal: <0.80 ng/ml) Electrocardiogram: No changes or signs of ischemia Transthoracic echocardiogram : Left ventricular ejection fraction 45–50% Akinesia in distal anteroseptal and apical segments Computed tomography coronary angiogram:mid‐to‐distal LAD dissected	Aspirin, Sublingual nitroglycerin
A 51-year-old female	Begining of chest pain after intense cough	Hypertension, tobacco use	ECG: mild ST segment elevation/ biphasic T waves in V2 and V3 Negative cardiac troponin Inconclusive echocardiography for myocardial ischemia Coronary angiography : SCAD at the distal left anterior descending artery (LAD)	Conservative treatment Dual antiplatelet therapy Anticoagulation Statin

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.

Electrocardiogram

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

X-ray

• There are no x-ray findings associated with COVID-19-associated spontaneous coronary artery dissection.
• To view the x-ray finidings on COVID-19, click here.
  

Echocardiography or Ultrasound

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

CT scan

• To view the CT scan findings on COVID-19, click here.

MRI

• To view the MRI findings on COVID-19, click here.
  

Other Imaging Findings

Coronary angiography

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

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 Therapy

• 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, along 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 the first choice if emergent revascularization is not necessary.
• To read more about PCI in Spontaneous Coronary Artery Dissection, Click here.

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.

Primary 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 procedures such as intubation or CPR.

Secondary Prevention

• There is no secondary measures for COVID-19-associated spontaneous coronary artery dissection.