Eur J Cardiothorac Surg 2002;22:777-780
© 2002 Elsevier Science NL
Post-infarction cardiac rupture: surgical treatment
Vittorio Mantovani*,
Davide Vanoli,
Paolo Chelazzi,
Vincenzo Lepore1,
Sandro Ferrarese,
Andrea Sala
Department of Cardiac Surgery, Ospedale di Circolo-Fondazione Macchi, Università dell'Insubria, Viale Borri 57, 21100 Varese, Italy
Received 28 May 2002;
received in revised form 20 July 2002;
accepted 23 July 2002.
* Corresponding author. Tel.: +39-347-464-2780; fax: +39-33-226-4394
e-mail: vitmantovani{at}hotmail.com
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Abstract
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Objective: Rupture of ventricular free wall (VFWR) may complicate acute myocardial infarction and accounts for high mortality. Surgical repair is the only therapeutic option. A review of our surgical experience is presented. Methods: Seventeen patients (11 men, mean age 68 years) underwent surgery for VFWR. Patch covering technique was used in 13 patients, infarctectomy with patch reconstruction in three patients, direct suture without patch in one patient. Coronary artery bypass grafting was performed in eleven patients. Results: Hospital mortality was 17.6% (three patients). Three patients died of cancer during the follow-up. The remaining 11 patients are in good condition after a mean follow-up of 45.8 months (range 7.584.2). Conclusions: Postinfarction rupture of ventricular free wall treated surgically gives excellent long-term results. Our first choice for repair is the covering technique with a large pericardial patch anchored with biological glue and epicardial sutures.
Key Words: Myocardial infarction Cardiac rupture Covering technique with pericardial patch
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1. Introduction
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Ventricular free wall rupture (VFWR) is an important but underrecognized cause of death after myocardial infarction (MI). The real incidence is unknown. Autopsy studies on in-hospital death for MI show a frequency of 724% [1,2]. There is general consensus that surgical repair is the only therapeutic option. We report our experience in 17 consecutive patients during a 14-year period.
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2. Patients and methods
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From January 1987 to December 2001, seventeen patients (mean age: 68±6 years; range: 5878) underwent surgical repair for VFWR. Eleven patients were male. Table 1 shows patients data, associated pathologies and preoperative drug treatment. The median interval between MI and rupture was 3 days (range 19). In nine patients (53%) the VFWR followed the first MI. Eleven patients (64%) had been treated conservatively for MI. Three patients received thrombolysis (18%) and three patients percutaneous transluminal coronary angioplasty (18%). In 16 patients the diagnosis of VFWR was made first by transthoracic echocardiography, in one case by ventriculography. Sixteen patients (94%) underwent coronary angiography. Three-vessels disease was present in five patients (29%), two-vessels disease in six patients (36%), and single-vessel disease in five patients (29%). For 16 patients, the median interval between rupture and surgery was 15 h (range 437). One patient, age 77, was operated on 14 days after the diagnosis of VFWR, when her condition worsened. All patients had inotropic agents at operation, and seven patients received an intra-aortic balloon pump preoperatively.
2.1. Follow-up
Follow-up information was obtained by direct contact with the patients. Follow-up at June 30, 2002 is 100% complete (mean follow-up: 45.8±6.6 months; range: 784).
2.2. Surgical technique
Surgery was performed with cardio-pulmonary bypass (CPB) and aortic cross-clamp (ACC). Cold crystalloid cardioplegia was used in six patients (35%) and cold blood cardioplegia in 11. The VFWR locations were in the antero-lateral wall in three patients (18%), in the lateral wall in three (18%), and in the postero-lateral wall in 11 (64%). In 13 patients the covering patch technique was employed, using either autologous or equinous pericardium. In 12 of them the patches were anchored to the heart surface by means of biological glue along with semi-continuous sutures in polypropylene. In one case the patch was fixed with glue only, avoiding the sutures. The type of glue mostly employed was gelatin-resorcin-formol (11 cases). In two patients fibrin glue was used (Tissucol, Baxter AG, Austria). In three cases an infarctectomy was performed, biological glue was not used and the reconstruction was carried out with pericardial patches. In one patient the site of rupture was directly sutured between felt strips, and pericardial patch was not employed.
Fourteen coronary artery bypass grafts (CABG) were performed in 11 patients. The five patients with one-vessel disease and the single patient without preoperative coronary angiogram did not undergo CABG. The left internal thoracic artery was used in three patients, all the other grafts being saphenous veins.
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3. Results
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Mean ACC time was 61±27 min. and mean CPB time was 108±37 min. In-hospital mortality was 17.6% (three patients). One patient suffered a papillary muscle rupture 7 days after surgery. He underwent mitral valve replacement and died 5 days thereafter for multi-organ failure. The second patient died after 13 days for acute renal failure and the last patient died of progressive cardiac failure, 25 days after surgery. One patient was reoperated after 1 day for subsequent ventricular septal rupture. He needed a third operation 3 months later for dehiscence of the septal patch. This was the only late cardiac reoperation, but not strictly related to the free wall repair. This patient died of cancer 34.7 months later.
During the follow-up, two other patients died of cancer respectively 34.4 and 79.3 months after surgery. No late cardiac deaths occurred and the 11 survivors are angina pectoris-free. Nine patients are in NYHA class I, two in class II. Table 2 shows the patients condition and Fig. 1
the KaplanMeier survival.
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4. Discussion
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Left ventricular free wall rupture is a life-threatening complication of acute MI. It occurs in 13% of all patients suffering from MI, accounting for up to one fourth of in-hospital deaths [24].
Several studies have shown risk factors such as age over 60 years, female sex and arterial hypertension [57]. The rupture occurs typically between 1 and 7 days after the infarction [6,810]. It might present suddenly with profound cardiogenic shock and cardiac tamponade. The rupture may otherwise occur as a two-stage event with a first phase of moderate pericardic effusion without shock and a later progression to a full-blown condition [5]. Park [11], Raitt [12] and Padro [13] used the term subacute cardiac rupture to describe this event, probably many more surgical series fall into this category. Veinot described a close proximity of rupture site with papillary muscle insertion[14]. Our findings seem to support this concept, as we observed most VFWRs in the postero-lateral wall.
The most important diagnostic tool for VFWR is transthoracic echocardiography, with sensitivity and specificity of the diagnosis reported between 93 and 98% [15].
Some studies suggest an association of VFWR with single vessel disease [16] and with first infarction [2,5,17]: both conditions might be related to poorly developed collateral circulation. In our experience multivessel coronary disease was present in the majority of patients, while first infarction was present in 53% of our cases. Only one patient in our series was on beta-blocking long-term treatment. It has been suggested that early beta-blocking treatment of MI might protect against VFWR [18] and Reddy [2] observed a low frequency of beta-blocking therapy among VFWR cases, even though the data are not complete.
Different opinions are published about the opportunity to perform coronary angiograms [19] or avoid this investigation in order to save time and to perform blind coronary artery bypass [10,20]. In our opinion a coronary angiogram should be promptly performed as soon as pericardial effusion is noted in MI patients, before they deteriorate. We believe, like other Authors [10], that a proper revascularization has a positive impact on survival and freedom from angina and our policy is to bypass major vessel with significant stenoses supplying non-infarcted areas. Two specific advantages of knowing the coronary status are seen in the covering technique. We use a very large patch, extended far beyond the necrotic area; the coronary arteries known to be healthy can be covered with minimal risk of needing a CABG in future; the knowledge of coronary status is of great help in deciding where and how placing the semi-continuous sutures. Our aim is to put a large number of shallow stitches along the whole patch margin.
Association of VFWR with thrombolytic treatment has been proposed by some studies [8,11,21], since plasmin, activated by thrombolytic drugs, has the known effect of breaking down collagen [22].
No moderate or severe mitral regurgitation was present preoperatively in our patients; postoperatively only two of them showed mild mitral regurgitation. We could not find in literature specific addresses to this topic, and our suggestion is not to treat mitral regurgitation unless its grade is moderate to severe.
Infarctectomy and direct suture techniques require full-depth stitches in healthy myocardium, since sutures on necrotic areas are likely to tear. This means a potential loss of viable myocardium. In the covering patch technique a large patch is securely anchored well beyond the ischemic area with shallow epicardial sutures that are unlikely to jeopardize the underlying healthy myocardium. We consider glue a mandatory complement to this technique, as described by Pretre [23] and Iemura [24]. Padro [13] reported excellent results by fixing the patch with glue only, as we did in one case, but he used always Teflon as covering material, while we feel more confident with pericardium. VFWR often develops as a result of myocardial dissection from the endocardial side towards epicardium. We underline the importance of using a very large patch: it might protect against the evolution of this dissection into new VFWR in areas close to the repair. We observed this progression of the rupture in two patients, unfortunately it took form of subsequent papillary muscle rupture and ventricular septal rupture.
In conclusion, surgical repair of post-ischemic free ventricular rupture is possible with acceptable early mortality and excellent long-term results. Coronary artery bypass grafting probably contributes to long-term symptom-free survival. Infarctectomy can be safely performed when needed, but our first choice is the covering technique, with a large pericardium patch anchored with biological glue and epicardial sutures.
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Footnotes
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1 Present address: Sahlgrenska University Hospital, Gothenburg, Sweden 
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