Myocardial rupture overview

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Myocardial rupture is a laceration or tearing of the walls of the ventricles or atria of the heart, of the interatrial or interventricular septum, of the papillary muscles or chordae tendineae or of one of the valves of the heart. It is most commonly seen as a serious sequelae of an acute myocardial infarction (heart attack).

Pathophysiology

The most common cause of myocardial rupture is a recent myocardial infarction, with the rupture typically occurring three to five days after infarction. Other causes of rupture include cardiac trauma, endocarditis (infection of the heart),[1][2] cardiac tumors, infiltrative diseases of the heart,[1] and aortic dissection.

Epidemiology and Demographics

The incidence of myocardial rupture has decreased in the era of urgent revascularization and aggressive pharmacological therapy for the treatment of an acute myocardial rupture. However, the decrease in the incidence of myocardial rupture is not uniform; there is a slight increase in the incidence of rupture if thrombolytic agents are used to abort a myocardial infarction.[3] On the other hand, if primary percutaneous coronary intervention is performed to abort the infarction, the incidence of rupture is significantly lowered.[4] The incidence of myocardial rupture if PCI is performed in the setting of an acute myocardial infarction is about 1 percent.[5]

Risk Factors

Risk factors for rupture after an acute myocardial infarction include female gender, advanced age of the individual, and a low body mass index. Other presenting signs associated with myocardial rupture include a pericardial friction rub, sluggish flow in the coronary artery after it is opened, the left anterior descending artery being the cause of the acute MI,[6] and delay of revascularization greater than 2 hours.

References

  1. 1.0 1.1 Lin TH, Su HM, Voon WC, Lai HM, Yen HW, Lai WT, Sheu SH. (2006). "Association between hypertension and primary mitral chordae tendinae rupture". Am J Hypertens. 19 (1): 75–9. PMID 16461195.
  2. de Diego C, Marcos-Alberca P, Pai RK. (2006). "Giant periprosthetic vegetation associated with pseudoaneurysmal-like rupture" (PDF). Eur Heart J. 27 (8): 912. PMID 16569654.
  3. Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, French WJ, Tiefenbrunn AJ, Bowlby LJ, Rogers WJ. (1996). "A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction". J Am Coll Cardiol. 27 (6): 1321–6. PMID 8626938.
  4. Moreno R, Lopez-Sendon J, Garcia E, Perez de Isla L, Lopez de Sa E, Ortega A, Moreno M, Rubio R, Soriano J, Abeytua M, Garcia-Fernandez MA. (2002). "Primary angioplasty reduces the risk of left ventricular free wall rupture compared with thrombolysis in patients with acute myocardial infarction". J Am Coll Cardiol. 39 (4): 598–603. PMID 11849857.
  5. Yip HK, Wu CJ, Chang HW, Wang CP, Cheng CI, Chua S, Chen MC. (2003). "Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era" (PDF). Chest. 124 (2): 565–71. PMID 12907544.
  6. Sugiura T, Nagahama Y, Nakamura S, Kudo Y, Yamasaki F, Iwasaka T. (2003). "Left ventricular free wall rupture after reperfusion therapy for acute myocardial infarction". Am J Cardiol. 92 (3): 282–4. PMID 12888132.


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