Spontaneous coronary artery dissection medical therapy: Difference between revisions

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==Overview==
==Overview==
There are no specific guidelines regarding the optimal management of [[spontaneous coronary artery dissection]]. Based on the [[clinical]] and [[angiographic]] scenario, treatment options include [[conservative medical regimens]] similar to that for [[acute coronary syndrome]], [[percutaneous coronary intervention]], and/or [[coronary artery bypass surgery]]. In the majority of cases, [[SCAD]] may be managed successfully with [[medical treatment]] alone in the absence of ongoing [[myocardial ischemia]] or [[hemodynamic instability]].
There are no specific guidelines regarding the optimal management of [[spontaneous coronary artery dissection]]. Based on the [[clinical]] and [[angiographic]] scenario, treatment options include [[conservative medical regimens]] similar to that for [[acute coronary syndrome]], [[percutaneous coronary intervention]], and/or [[coronary artery bypass surgery]]. In the majority of cases, [[SCAD]] may be managed successfully with [[medical treatment]] alone in the absence of ongoing [[myocardial ischemia]] or [[hemodynamic instability]].
Initial [[conservative]] management typically includes [[antithrombotic therapy]] with [[heparin]], [[aspirin]], [[clopidogrel]] and [[glycoprotein IIb/IIIa inhibitors]], and antiischemic therapy with [[beta blockers]] and [[nitrate]]s.  However, the use of [[antithrombotic]] therapy may increase the risk of bleeding in the [[false lumen]] causing an expansion of the [[intramural hematoma]], resulting in a decreased [[flow]] through the [[true lumen]].[[Fibrinolytic]]s should be avoided. [[Calcium channel blocker]]s may offer relief in [[coronary artery spasm]].
Initial [[conservative]] management typically includes [[antithrombotic therapy]] with [[heparin]], [[aspirin]], [[clopidogrel]] and [[glycoprotein IIb/IIIa inhibitors]], and antiischemic therapy with [[beta blockers]] and [[nitrate]]s.  However, the use of [[antithrombotic]] therapy may increase the risk of bleeding in the [[false lumen]] causing an expansion of the [[intramural hematoma]], resulting in a decreased [[flow]] through the [[true lumen]].[[Fibrinolytic]]s should be avoided. [[Calcium channel blocker]]s may offer relief in [[coronary artery spasm]].


==Medical Therapy==
==Medical Therapy==

Revision as of 12:35, 3 March 2021

Spontaneous Coronary Artery Dissection Microchapters

Home

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Spontaneous coronary artery dissection from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Approach

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Angiography

CT

MRI

Echocardiography

Other Imaging Findings

Other Diagnostic Studies

Treatment

Treatment Approach

Medical Therapy

Percutaneous Coronary Intervention

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Type 1

Type 2A

Type 2B

Type 3

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nate Michalak, B.A. Arzu Kalayci, M.D. [2]

Synonyms and keywords: SCAD

Overview

There are no specific guidelines regarding the optimal management of spontaneous coronary artery dissection. Based on the clinical and angiographic scenario, treatment options include conservative medical regimens similar to that for acute coronary syndrome, percutaneous coronary intervention, and/or coronary artery bypass surgery. In the majority of cases, SCAD may be managed successfully with medical treatment alone in the absence of ongoing myocardial ischemia or hemodynamic instability. Initial conservative management typically includes antithrombotic therapy with heparin, aspirin, clopidogrel and glycoprotein IIb/IIIa inhibitors, and antiischemic therapy with beta blockers and nitrates. However, the use of antithrombotic therapy may increase the risk of bleeding in the false lumen causing an expansion of the intramural hematoma, resulting in a decreased flow through the true lumen.Fibrinolytics should be avoided. Calcium channel blockers may offer relief in coronary artery spasm.

Medical Therapy

Beta Blockers

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. [4] Furthermore, beta blockers should be used in these group of patients in order to reduce complications of myocardial infarction. [5] [6]

Antiplatelet Therapy

Although there is no evidence for using long term anti platelet therapy in this specific group of patients, it is reasonable to use aspirin for acute and long term management with considering acute coronary syndrome as an indication.[7] It remains controversial to use clopidogrel in patients managed with conservative therapy. However, it seems to be beneficial to use clopidogrel in acute management to avoid a new thrombus formation in true lumen on the basis of dissected part and to reduce the thrombus burden in the false lumen. [8] The effects of P2Y12 antagonists (ticagrelor and prasugrel) in management of SCAD patients is not clear. In addition, glycoprotein IIb/IIIa inhibitors should be avoided in these patients because of high risk of bleeding and a potential risk of extending the dissection. [9]

Anticoagulant and Thrombolytic Therapy

The role of anticoagulants in SCAD is still in question. It is one of the standard therapy in acute coronary syndrome but it has both advantages and disadvantages in SCAD patients. Even though anticoagulation poses a treat for extension of the dissection, it seems to be beneficial for preventing from further thrombi formation and keeping the true lumen patent. Thrombolytic therapy has been reported as harmful due to the enlargement of intramural haematom and dissection. [10] [11]

Angiotensin-Converting Enzyme Inhibitor or Angiotensin Receptor Blocker

According to the current guidelines, angiotensin converting enzyme inhibitors and angiotensin receptor blockers are strongly recommended for patients with acute myocardial infarction associated with heart failure, impaired left ventricular systolic functions or preserved left ventricular systolic function. [12] There is no consensus in the literature about the benefits of these agents in patients with SCAD. However, there is an ongoing, randomized controlled study regarding the effects of angiotensin-converting enzyme inhibitors and statins in SCAD patients (SAFER-SCAD - NCT02008786)

Statins

The role of statins in SCAD is still unknown. It has been claimed that there could be potential harm of statins in SCAD patients. [2] However when it has been evaluated in SCAD patients with myocardial infarction, a significant benefit was determined. [6] Since atherosclerosis is not the underlying mechanism, it seems to be reasonable to use statins in patients who have also hyperlipidemia in these group of patients.

Antianginal Therapy

Antianginal therapies with nitrates, calcium channel blockers, or ranolazine may be considered for post-SCAD chest pain syndromes in patients who are not candidates for revascularization or who have evidence suggesting coronary vasospasm or coronary microvascular dysfunction. While antianginal therapy is effective in relieving ischemic symptoms, the use must be balanced with potential adverse reactions, most commonly symptomatic hypotension and headache. Routine administration of antianginal therapy for either the index SCAD hospitalization or long term is not recommended.[13]

References

  1. Saw J, Aymong E, Sedlak T, Buller CE, Starovoytov A, Ricci D; et al. (2014). "Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes". Circ Cardiovasc Interv. 7 (5): 645–55. doi:10.1161/CIRCINTERVENTIONS.114.001760. PMID 25294399.
  2. 2.0 2.1 Tweet MS, Hayes SN, Pitta SR, Simari RD, Lerman A, Lennon RJ; et al. (2012). "Clinical features, management, and prognosis of spontaneous coronary artery dissection". Circulation. 126 (5): 579–88. doi:10.1161/CIRCULATIONAHA.112.105718. PMID 22800851.
  3. Vrints, CJ. (2010). "Spontaneous coronary artery dissection". Heart. 96 (10): 801–8. doi:10.1136/hrt.2008.162073. PMID 20448134.
  4. Nienaber CA, Powell JT (2012). "Management of acute aortic syndromes". Eur Heart J. 33 (1): 26–35b. doi:10.1093/eurheartj/ehr186. PMID 21810861.
  5. Mehta LS, Beckie TM, DeVon HA, Grines CL, Krumholz HM, Johnson MN; et al. (2016). "Acute Myocardial Infarction in Women: A Scientific Statement From the American Heart Association". Circulation. 133 (9): 916–47. doi:10.1161/CIR.0000000000000351. PMID 26811316.
  6. 6.0 6.1 Amsterdam EA, Wenger NK, Brindis RG, Casey DE, Ganiats TG, Holmes DR; et al. (2014). "2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". Circulation. 130 (25): 2354–94. doi:10.1161/CIR.0000000000000133. PMID 25249586.
  7. Antithrombotic Trialists' Collaboration (2002). "Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients". BMJ. 324 (7329): 71–86. PMC 64503. PMID 11786451. Review in: ACP J Club. 2002 Jul-Aug;137(1):5
  8. Choi JW, Davidson CJ (2002). "Spontaneous multivessel coronary artery dissection in a long-distance runner successfully treated with oral antiplatelet therapy". J Invasive Cardiol. 14 (11): 675–8. PMID 12403896.
  9. Saw J (2013). "Spontaneous coronary artery dissection". Can J Cardiol. 29 (9): 1027–33. doi:10.1016/j.cjca.2012.12.018. PMID 23498840.
  10. Shamloo BK, Chintala RS, Nasur A, Ghazvini M, Shariat P, Diggs JA; et al. (2010). "Spontaneous coronary artery dissection: aggressive vs. conservative therapy". J Invasive Cardiol. 22 (5): 222–8. PMID 20440039.
  11. Zupan I, Noc M, Trinkaus D, Popovic M (2001). "Double vessel extension of spontaneous left main coronary artery dissection in young women treated with thrombolytics". Catheter Cardiovasc Interv. 52 (2): 226–30. PMID 11170335.
  12. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE, Colvin MM; et al. (2017). "2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America". J Card Fail. 23 (8): 628–651. doi:10.1016/j.cardfail.2017.04.014. PMID 28461259.
  13. Hayes, Sharonne N.; Kim, Esther S.H.; Saw, Jacqueline; Adlam, David; Arslanian-Engoren, Cynthia; Economy, Katherine E.; Ganesh, Santhi K.; Gulati, Rajiv; Lindsay, Mark E.; Mieres, Jennifer H.; Naderi, Sahar; Shah, Svati; Thaler, David E.; Tweet, Marysia S.; Wood, Malissa J. (2018). "Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association". Circulation: CIR.0000000000000564. doi:10.1161/CIR.0000000000000564. ISSN 0009-7322.