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Ann Thorac Surg 2002;74:101
© 2002 The Society of Thoracic Surgeons
a 70 Shagbark Court, Iowa City, IA 52246, USA
Each year in the United States over a half million individuals die of acute myocardial infarction. Epidemiology studies based on autopsies indicate that 8% to 24% of these deaths are a result of myocardial free wall rupture [1, 2]. In the current era, it seems implausible that this high incidence still exists. Causative factors such as hypertension, heart rate, preload, afterload, and inotropic state are routinely addressed in the coronary care unit. Early reperfusion by balloon dilatation or fibrinolytics has been demonstrated to preserve myocardial function, a factor undoubtably related to limitation of infarct size and depth [3]. Early studies with fibrinolytics did suggest a decreased incidence of rupture when they were employed within the first 5 hours of infarct [4] with a higher incidence if they were administered late. Subsequent reports failed to confirm the higher incidence but did suggest that the time course to rupture might be accelerated when antifibrinolytics are employed [5]. Indirect evidence also suggests that current rates of rupture are probably considerably lower than previously reported. Were the rupture rate to approach even 10%, cardiac surgeons should have an abundance of opportunity to encounter this condition. Yet, even at high volume centers, only 1 to 3 cases per year are identified. Thus, for most cardiac surgeons, it is rare to encounter the condition, and for them there is virtually no opportunity to develop a standardized technique to handle such an emergency when it develops.
The textbook approach for this condition is excision of the infarcted zone and replacement with a suitable prosthetic patch. This description of the procedure is disarming since rarely, if ever, does one find a simple "blow-out" with normal muscle surrounding the defect. In at least half of the cases, the endocardial defect is relatively small while the blood takes a circuitous route through damaged myocardium to exit through multiple rents on the epicardium. A bleeding hematoma is a better description than free wall rupture. One must make numerous critical choices: First, would it be possible to control the area with multiple buttressed sutures? Will this cause further bleeding and aggravate the presentation? If resection of the hematoma is chosen, how large of an area needs to be resected, and how does one determine that with a muscle swollen and infused with blood? Finally, how is the patch to be attached? Will anchoring the patch further damage adjacent myocardium? Too often the simplest procedure is tried initially with each step gradually proceeding to the creation of a "Teflon" ventricle. Mortality rates from this approach are generally in the 25% to 30% range [6], although it can be inferred that mortality is considerably higher since most unsuccessful repairs are never reported.
An intriguing method to control left ventricular rupture is reported in this issue of The Annals by Lachhapelle and colleagues. He describes the use of a sutureless patch technique employing a biocompatible glue. The technique is intriguing since the procedure was employed in 6 consecutive cases with the bleeding controlled in all. Lachapelle’s article builds on a previous report by Padro [7], who in 1993 reported on 13 cases, all with a successful result. The methodology is simple and easily employed and appears capable of controlling even active hemorrhage if combined with cardiopulmonary bypass.
Obviously, there are instances in which this technique is inadequate. Ventricular septal defect occurs in about 12% of all patients with free wall rupture; and for these patients, the traditional approach or the endocardial patch with infarct exclusion as described by David [8] is required. However, for about 85% of all free wall ruptures encountered, this technique seems promising.
References
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