Postinfarction Ventricular Septal Rupture

Postinfarction Ventricular Septal Rupture

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Ventricular septal rupture (VSR) is a rare but lethal complication of myocardial infarction (MI). The event occurs 2-8 days after an infarction and often precipitates cardiogenic shock. [1]  The differential diagnosis of postinfarction cardiogenic shock should exclude free ventricular wall rupture and rupture of the papillary muscles. (See the image below.)

To avoid the high morbidity and mortality associated with this disorder, patients should undergo emergency surgical treatment. [2, 3, 4, 5]  In current practice, postinfarction VSR is recognized as a surgical emergency, and the presence of cardiogenic shock is an indication for intervention. [6]  Long-term survival can be achieved in patients who undergo prompt surgery. Concomitant coronary artery bypass grafting (CABG) may be required. The addition of CABG has helped improve long-term survival.

Surgery is performed via a transinfarction approach, and all reconstruction is performed with prosthetic materials to avoid tension. Developments in myocardial protection and improved prosthetic materials have contributed greatly to successful management of VSR. [7]  Improved surgical techniques (eg, infarctectomy) and better perioperative mechanical and pharmacologic support have helped lower mortality. In addition, the development of surgical techniques to repair perforations in different areas of the septum has led to improved results.

In current practice, patients undergoing shunt repair tend to be older and are more likely to have received thrombolytic agents, which may complicate repair. After successful repair, survival and quality of life are excellent, even in patients older than 70 years. [8]

For information, news, and CME activities on heart failure, see the Heart Failure Resource Center. For patient education resources, see the Heart Center, as well as Ventricular Septal Defect and Heart Attack.

The septal blood supply comes from branches of the left anterior descending coronary artery, the posterior descending branch of the right coronary artery, or the circumflex artery when it is dominant. Infarction associated with a VSR is usually transmural and extensive. About 60% of VSRs occur with infarction of the anterior wall, 40% with infarction of the posterior or inferior wall (see the image below). Posterior VSR may be accompanied by mitral valve insufficiency secondary to papillary muscle infarction or dysfunction.

At autopsy, patients with VSR usually show complete coronary artery occlusion with little or no collateral flow. The lack of collateral flow may be secondary to associated arterial disease, anatomic anomalies, or myocardial edema. Sometimes, multiple septal perforations occur. These may occur simultaneously or within several days of each other.

Ventricular aneurysms are commonly associated with postinfarction VSR and contribute significantly to the hemodynamic compromise in these patients. The reported incidence of ventricular aneurysms ranges from 35% to 68%, whereas the incidence of ventricular aneurysms alone after MI without VSR is considerably lower (12.4%).

The natural history of postinfarction VSR is greatly influenced by hypertension, anticoagulation therapy, advanced age, and, possibly, thrombolytic therapy. The natural course in patients with postinfarction VSR is well documented and short. Most patients die within the first week, and almost 90% die within the first year; some reports indicate that fewer than 7% of patients are alive after 1 year.

This grim prognosis results from an acute volume overload exacted on both ventricles in a heart already compromised by a large MI and occasionally by extensive coronary artery disease (CAD) in sites other than that already infarcted. In addition, superimposed ischemic mitral valve regurgitation, a ventricular aneurysm, or a combination of these conditions may be present, further compromising heart function. The depressed left ventricular function commonly leads to impaired peripheral organ perfusion and death in most patients.

A few sporadic reports indicate that some patients with medically treated postinfarction VSR live for several years. Although many medical advances have been made in the nonsurgical treatment of these patients, including intra-aortic balloon counterpulsation (IABCP), these methods have not eliminated the need for surgery.

Rupture of the interventricular septum is an uncommon complication of MI. Although autopsy studies reveal an 11% incidence of myocardial free-wall rupture after MI, septal-wall perforation is much less common, occurring at a rate of approximately 1-2%.

VSR occurs in a zone of necrotic myocardial tissue, usually within the first 10-14 days. Clinical studies report an average time of 2.6 days from MI to VSR. However, some data suggest that initial treatment of MI with thrombolytics may affect both the time between infarction and VSR and the eventual outcome. Early use of thrombolytic agents may lead to reopening of the occluded vessels, thereby reducing the incidence of VSR.

The age range of patients who sustain a postinfarction VSR is wide, from 44 to 81 years. Men are affected more commonly than women are, though VSR is more common in women than would be predicted on the basis of the prevalence of CAD alone.

Operative mortality is directly related to the interval between MI and surgical repair. In a retrospective analysis of 41 patients treated for postinfarction ventricular septal defect (VSD), Serpytis et al confirmed that whereas female sex, advanced age, arterial hypertension, anterior-wall acute MI, absence of previous acute MI, and late arrival at hospital were associated with a higher risk of mortality from acute VSD, the time from the onset of acute MI to operation was the most important factor determining operative mortality and intrahospital survival. [9]

If repair of a postinfarction VSR is performed 3 weeks or more after the infarction, mortality is approximately 20%; if it is performed before this time, mortality approaches 50%. The most obvious reason for this is that the greater the degree of myocardial damage and hemodynamic compromise, the more urgent the need for early intervention.

With the use of an early operative approach, most studies show an overall mortality of less than 25%. Mortality tends to be lower for patients with anteriorly located VSRs and lowest for patients with apical VSRs. For anterior defects, mortality ranges from 10% to 15%; for posterior defects, mortality ranges from 30% to 35%.

More than 50% of deaths occurring after surgery for postinfarction VSR are due to cardiac failure. Sudden death is rare, and intractable heart failure can also occur. Other causes of death include cerebral embolism. Most patients who survive the hospital period have good functional status, with the majority falling into New York Heart Association (NYHA) class I or II. [10]

The most important risk factors for death in the early phase are poor hemodynamics and associated right ventricular dysfunction developing before the patient comes to the operating room. The amount and distribution of myocardial necrosis and scarring are responsible for both.

Right ventricular dysfunction results from ischemic damage or frank infarction of the right ventricle and is present when stenosis occurs in the right coronary artery system. The higher mortality observed after repair of defects located inferiorly in the septum is probably related to the higher prevalence of important right coronary artery stenosis.

The severity and distribution of CAD are also risk factors. Similarly, advanced age at operation, diabetes, and preinfarction hypertension are risk factors for death in the early phase.

Risk factors for death in patients with postinfarction VSR may be summarized as follows:

In a retrospective analysis of 52 consecutive patients with surgically repaired postinfarction VSR over a 30-year period (mean follow-up, 7.8±7.7 years), Takahashi et al found that predictors of 30-day mortality on univariate analysis included the following [11] :

On multivariate analysis, only incomplete coronary revascularization was an independent risk factor for 30-day mortality. [11]

Koh AS, Loh YJ, Lim YP, Le Tan J. Ventricular septal rupture following acute myocardial infarction. Acta Cardiol. 2011 Apr. 66(2):225-30. [Medline].

David TE. Operative management of postinfarction ventricular septal defect. Semin Thorac Cardiovasc Surg. 1995 Oct. 7(4):208-13. [Medline].

Gaudiani VA, Miller DG, Stinson EB, et al. Postinfarction ventricular septal defect: an argument for early operation. Surgery. 1981 Jan. 89(1):48-55. [Medline].

Roberts JD, So DY, Lambert AS, Ruel M. Successful surgical repair of ventricular double rupture. Can J Cardiol. 2011 Nov. 27(6):868.e5-7. [Medline].

Kuthe SA, Mohite PN, Sarangi S, Mathews S, Thingnam SK, Reddy S. Repair of postinfarct ventricular septal defect and total myocardial revascularization in a case of dextrocardia with situs inversus. Gen Thorac Cardiovasc Surg. 2011 Jan. 59(1):42-4. [Medline].

Heitmiller R, Jacobs ML, Daggett WM. Surgical management of postinfarction ventricular septal rupture. Ann Thorac Surg. 1986 Jun. 41(6):683-91. [Medline].

Daggett WM, Buckley MJ, Akins CW, et al. Improved results of surgical management of postinfarction ventricular septal rupture. Ann Surg. 1982 Sep. 196(3):269-77. [Medline].

Muehrcke DD, Daggett WM. Current surgical approach to acute ventricular septal rupture. Adv Card Surg. 1995. 6:69-90. [Medline].

Serpytis P, Karvelyte N, Serpytis R, Kalinauskas G, Rucinskas K, Samalavicius R, et al. Post-infarction ventricular septal defect: risk factors and early outcomes. Hellenic J Cardiol. 2015 Jan-Feb. 56(1):66-71. [Medline].

Cummings RG, Califf R, Jones RN, et al. Correlates of survival in patients with postinfarction ventricular septal defect. Ann Thorac Surg. 1989 Jun. 47(6):824-30. [Medline].

Takahashi H, Arif R, Almashhoor A, Ruhparwar A, Karck M, Kallenbach K. Long-term results after surgical treatment of postinfarction ventricular septal rupture. Eur J Cardiothorac Surg. 2015 Apr. 47(4):720-4. [Medline].

Deja MA, Szostek J, Widenka K, et al. Post infarction ventricular septal defect – can we do better?. Eur J Cardiothorac Surg. 2000 Aug. 18(2):194-201. [Medline].

Okamoto Y, Yamamoto K, Asami F, Kimura M, Mizumoto M, Okubo Y, et al. Early and midterm outcomes of triple patch technique for postinfarction ventricular septal defects. J Thorac Cardiovasc Surg. 2016 Jun. 151 (6):1711-6. [Medline].

Arnaoutakis GJ, Zhao Y, George TJ, et al. Surgical repair of ventricular septal defect after myocardial infarction: outcomes from the Society of Thoracic Surgeons National Database. Ann Thorac Surg. 2012 Aug. 94(2):436-43; discussion 443-4. [Medline].

Stolt V, Cook S, Raber L, et al. Amplatzer Septal Occluder to treat iatrogenic cardiac perforations. Catheter Cardiovasc Interv. 2012 Feb 1. 79(2):263-70. [Medline].

Schlotter F, de Waha S, Eitel I, Desch S, Fuernau G, Thiele H. Interventional post-myocardial infarction ventricular septal defect closure: a systematic review of current evidence. EuroIntervention. 2016 May 17. 12 (1):94-102. [Medline]. [Full Text].

Shabir Bhimji, MD, PhD Cardiothoracic and Vascular Surgeon, Saudi Arabia and Middle East Hospitals

Shabir Bhimji, MD, PhD is a member of the following medical societies: American Cancer Society, American College of Chest Physicians, American Lung Association, Texas Medical Association

Disclosure: Nothing to disclose.

Brett C Sheridan, MD, FACS Associate Professor of Surgery, University of North Carolina at Chapel Hill School of Medicine

Disclosure: Nothing to disclose.

Shreekanth V Karwande, MBBS Chair, Professor, Department of Surgery, Division of Cardiothoracic Surgery, University of Utah School of Medicine and Medical Center

Shreekanth V Karwande, MBBS is a member of the following medical societies: American Association for Thoracic Surgery, American College of Chest Physicians, American College of Surgeons, American Heart Association, Society of Critical Care Medicine, Society of Thoracic Surgeons, and Western Thoracic Surgical Association

Disclosure: Nothing to disclose.

Jeffrey C Milliken, MD Chief, Division of Cardiothoracic Surgery, University of California at Irvine Medical Center; Clinical Professor, Department of Surgery, University of California, Irvine, School of Medicine

Jeffrey C Milliken, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American College of Cardiology, American College of Chest Physicians, American College of Surgeons, American Heart Association, American Society for Artificial Internal Organs, California Medical Association, International Society for Heart and Lung Transplantation, Phi Beta Kappa, Society of Thoracic Surgeons, Southwest Oncology Group, and Western Surgical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Postinfarction Ventricular Septal Rupture

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