POST INFARCT VSR AND ITS RECENT UPDATES

PRESENTERDR A.Y.M. SHAHIDULLAH MS STUDENT MODERATORDR. RAMPADA SARKER ASST. PROFESSOR DEPT. OF CARDIAC SERGURY NICVD

DEFINITION

Post infarct ventricular septal rupture (VSR) is a defect in the ventricular septum that results from rupture of acutely infarcted myocardium.

History

In 1845, Latham described a postinfarction ventricular septal rupture at autopsy. In 1923, Brunn first made the diagnosis antemortem. In 1934, Sager added the 18th case to the world literature and established specific clinical criteria for diagnosis. In 1956, Cooley and associates performed the first successful surgical repair in a patient 9 weeks after the diagnosis of septal rupture.

Incidence

Approximately 1% to 2% of cases of acute myocardial infarctions (AMI) results in VSR and account for about 5% of early deaths. The average time from infarction to rupture is between 2 and 4 days, but it may be as short as a few hours or as long as 2 weeks.

Post infarction VSR occur in men more often than

women (3 to 2).

Pathogenesis

Slippage of myocytes during infarct expansion allow blood to dissect through the necrotic myocardium and enter either the right ventricle or pericardial space. Hyaline degeneration of cardiomyocytes with subsequent fragmentation and enzymatic digestion allow fissures to form, predisposing to rupture. Post infarction ventricular rupture usually associated with complete occlusion rather than severe stenosis of a coronary artery.

Types of VSR

Simple: It consists of a direct through-and-through defect, located anteriorly, in approximately 60% of cases, following occlusion of the left anterior descending artery.

Complex: It consists of a serpiginous dissection tract remote from the primary septal defect, located inferiorly, about 20% to 40% of patients.

Pathophysiology
Acute Ventricular Infarction Acute Myocardial Infarction

Ventricular Septal Rupture

Ventricular Dysfunction

Acute Left To Right Shunt

Heart Failure ( Rt or Lt or Both)

Cardiogenic Shock

Multi Organ Failure

Natural History

Mortality of postinfarction septal rupture without surgical intervention About 25% within the first 24 hours, About 50% within 1 week, About 65% within 2 weeks, About 80% within 4 weeks and Only 7% lived longer than one year.

Diagnosis

The typical presentation of a ventricular septal rupture - A new loud , harsh, pansystolic murmur ( 90% of cases) best heard at the left lower sternal border, associated with a palpable thrill - Recurrent chest pain, - An abrupt deterioration in hemodynamics.

cont.

Diagnosis

ECG findings- changes associated with antecedent anterior, inferior, posterior or septal infarction, A-V conduction block. Echocardiography findingsThe defect, Site and size, Right and left ventricular function, Pulmonary artery and right ventricular pressures, and Exclude coexisting mitral regurgitation or free wall rupture. Left heart catheterizationcoronary artery disease, left ventricular wall motion, and specifics of valvular dysfunction.

Preoperative Management

The goals- To reduce the systemic vascular resistance, thus the left-to-right shunt; - To maintain cardiac output and arterial pressure to ensure peripheral organ perfusion; - To maintain or improve coronary artery blood flow.
These are best accomplished by the intra-aortic balloon pump (IABP). Counterpulsation reduces left ventricular afterload, thereby increasing cardiac output and decreasing the left-to-right shunt Thus- decreased myocardial oxygen consumption, - improved myocardial and peripheral organ perfusion.

Pharmacologic therapy- Inotropic agents - Diuretics - Vasodilators.

Principles of repair of postinfarction ventricular septal defects-

Cardiopulmonary bypass with moderate hypothermia and meticulous myocardial protection.

Transinfarct approach to ventricular septal defect with the site of ventriculotomy determined by the location of the transmural infarction. Trimming of the left ventricular margins of the infarct back to viable muscle to prevent delayed rupture of the closure site. Conservative trimming of the right ventricular muscle as required for complete visualization of the margins of the defect.

Cont

Inspection of the left ventricular papillary muscles and concomitant replacement of the mitral valve only if there is frank papillary muscular rupture. Closure of the septal defect without tension, with the use of prosthetic material. Closure of the infarctectomy without tension with the use of prosthetic material and epicardial placement of the patch to the free wall to avoid strain on the friable endocardial tissue. Buttressing of the suture lines with pledgets or strips of Teflon felt or similar material to prevent sutures from cutting through friable muscle.

Repair of anterior post infarction VSD

Pledgeted sutures are taken from VSD margin to patch margin

Continuous instead of interrupted sutures

Ventriculotomy closure with suture over felt

continuous suture for reinforcement

INFARCT EXCLUSION TECHNIQUE

Left ventricular cavity excluded from infarcted myocardium

Oval bovine pericardial patch sutured to endocardium over noninfarcted ventricular septum

REPAIR OF POSTINFARCTION VSD IN APICAL PORTION

Infarcted portion of both ventricles are excised with VSD

Closure for apex using PTFE felt

REPAIR OF POSTERIOR POST INFARCTION VSD

Second patch is used to close RV wall

Heart is lifted out of pericardial cavity

Infarcted tissue of LV, RV & septum are excised

Septal patch is placed on LV side External patch is placed over infarcted area

INFARCT EXCLUSION TECHNIQUE

Lateral edge of patch is sutured to LV wall near post papillary muscle

Left ventriculotomy is done

Bovine patch is sutured on healthy portion of LV starting on fibrous mitral anulus

Exclude all infarcted muscle of LV cavity

. Surgery for post-infarction ventricular septal defect (VSD): double

patch and glue technique for early repair
Claude Deville*, Louis Labrousse,Emmanuel Choukroun and Francesco Madonna

Department of Cardio-Vascular Surgery, Hpital Haut-Lvque, avenue de Magellan, 33604 Bordeaux-Pessac, France

Site of ventriculotomies close to the septal margin.

Double ventriculotomy in one case of anterior VSD.

Right side of ventricular septum with ventricular septal defect, tricuspid papillary muscle tip on moderator band.

Patch on the right side of the ventricular septum preserving important anatomical structures.

Septal surface of the left ventricle presenting only fine trabeculations.

Patch on the left side of the ventricular septum.

Patches crossing the ventriculotomies

Dacron patch on each side of the septum and glue injection.

Strip of felt on the right and left ventricular sides of the incisions.

Simultaneous closure of the two ventriculotomies with heavy mattressed and transseptal suture

The interrupted stitches suture closing the two ventriculotomies.

Results-

No recurrences of VSD was observed in 37 patients operated on with this technique since 1986, compared to six recurrences in the 56 patients operated with the classic repair, P=0.09. This confirms our previous results published in 2002 . Hospital mortality with the double patch and glue techniqueconcerns 10 out of 37 patients (27%) compared to 28 among 56patients (50%) with the classic repair, P=0.006

Double-Patch Repair of Postinfarction Ventricular Septal Defect

Mehmet Balkanay, MD, Ercan Eren, MD, Cuneyt Keles, MD, Mehmet Erdem Toker, MD, and Mustafa Guler, MD
Department of Cardiovascular Surgery, Kosuyolu Heart and Research Hospital, Istanbul, Turkey

The ventricular septal perforation was closed directly by stitching, with the same sutures, 2 autologous pericardial patches onto both sides of the affected septum, through only a left ventriculotomy. Complete closure of the defect was accomplished, and no residual shunt was observed in any patient.

A) A longitudinal transinfarction incision is made in the left ventricular myocardium parallel to and 10 mm away from the posterior descending artery. B) Several 3-0 Prolene sutures are passed through the 1st pericardial patch; then the needles are passed transmurally by everting them through the healthy portion of the defect, from the right side of the septum to the left. C)1st patch is lowered to the right side of the defect by tying the sutures tightly; then the needles of the same sutures are passed through the 2nd pericardial patch. D) All these sutures are then tied securely on the left side of the septum, thus closing the defect completely on both sides, with a double patch.

Off-pump repair of a post-infarct ventricular septal defect: the 'Hamburger procedure'

Thomas A Barker, Alexander Ng, and Ian S Morgan
Department of Cardiothoracic Surgery, Heart and Lung Centre, Wolverhampton, UK Department of Cardiothoracic Anaesthesia, Critical Care & Pain Management, Heart and Lung Centre, Wolverhampton, UK

An off-pump closure technique called the 'Hamburger procedure' has been pioneered as an alternative to open procedures that require CPB and ventriculotomy.

By bringing the left and right ventricles into close apposition with Teflon supported plication sutures, the defect was closed with moderate reductions in cardiac chamber size.

A dramatic reduction in pulmonary arterial pressure and inotropic doses occurred immediately after surgery. As this technique was performed off-pump, potential sequelae of CPB (ie adverse haemodynamic, neurological and inflammatory effects) were obviated. A short operative time of 40 minutes compared with a longer, more complex open patch repair requiring CPB and ventriculotomy.

ASSOCIATED PROCEDURES

- Concomitant coronary artery bypass - Mitral valve replacement - Left ventricular aneurysm - Repair of free wall rupture

Operative Mortality

Hospital mortality after repair is 30% to 50%. Five year survival 44% - 57%. Ten year survival 29% - 36%. Modes of deathEarly- Cardiac failure (up to 90%), Bleeding, Sepsis, Stroke, GIT bleeding Recurrent VSD.

Late-

Cardiac failure, Sudden death, Sepsis, Stroke MI

INDICATION FOR OPERATION

Post infarction VSD is almost always an indication for operation. Repair of post infarction VSD 2 to 3 weeks or more after septal rupture is relatively safe. Operation can be delayed if- adequate cardiac output with no evidence of shock - easy controllable or absence of symptoms of pulmonary venous hypertension - easy controllable or absence of fluid retention - good renal function

PERCUTANEOUS CLOSURE
Successful transcatheter closure of postinfarction ventricular septal rupture has been reported using several types of catheter-deployed devices- CardioSEAL device, double umbrella prosthesis. - Amplatzer septal occluder and

- Rashkind double umbrella.

Results of early repair of post infarction VSR in literature

source: MMCTS (April 25, 2005) Year Author No. of Pt Mean delay in surgery (day) 5-6 2 3 2 Location of VSD Ant % 50 42 59 50 69 44.5 Location of VSD Post % 50 58 41 50 31 55.5 Hospital mortality % 27.5 32 32 19 37 26 Recurrence of VSD % 22.9 6 5.7 43 -

1996 1998 1998 1998 1999 1999

Cox Chaux Dalrymplehay David Deja Prete

109 31 150 52 110 54

2000 2003
2004

Crenshaw Barker
Daville
one patch two patch

84 65
56 37

3.5 11.5
3.4 3.1

71.5 46
55.5 59.5

28.5 54
44.5 40.5

47 23.1
50 27

7 0

Surgical repair of post-infarction ventricular septal defect: 19 years of experience

Vittorio Mantovani, , Giovanni Mariscalco, Cristian Leva, Claudio Blanzola and Andrea Sala

Department of Cardiac Surgery, Ospedale di Circolo-Fondazione Macchi, Universit dell'InsubriaViale Borri 57, 21100 Varese, Italy
Received 10 November 2004;

Objectives To review our experience of surgical repair of post-infarction ventricular septal defect (VSD). Methods In the period 19832002, 50 patients underwent repair of VSD. Mean age was 66 years, male sex 52%. Infarct location was anterior in 60% and posterior in 40% of cases. Median interval between rupture and surgery was 2 days. Preoperative intra-aortic balloon counterpulsation was employed in 56%; a coronary angiogram was performed in 98% of cases. A patch repair technique was used in 90% of cases. Coronary bypass grafting was associated in 50% of patients. Results Mean aortic clamp time was 101 31 min. Global operative mortality was 36%, respectively 26.7% in anterior and 50% in posterior location (p = ns). Emergency operation and interval from rupture to surgery less than 3 days were univariate predictor of early mortality. Five years survival excluding operative deaths was 76%. Conclusions The surgical repair of post-infarction VSD entails a high operative mortality; different techniques were employed with similar results. Emergency operation is associated with a worse short-term prognosis; long-term survival is acceptable.

Long-Term Results After Surgical Repair of Postinfarction Ventricular Septal Rupture by Infarct Exclusion Technique
Nestoras Papadopoulos MD, Anton Moritz MD, PhD, Omer Dzemali MD, Andreas Zierer MD, Amin Rouhollapour MD, Hanns Ackermann PhD and Farhad Bakhtiary MD, PhD

Department of Thoracic and Cardiovascular Surgery, Johann-Wolfgang-Goethe University Hospital, Frankfurt/Main, Germany Center of Health Science, Institute for Biostatistics and Mathematical Modelling, Johann Wolfgang-Goethe University Hospital, Frankfurt/Main, germany

Background
Ventricular septal defect (VSD) is one of the most serious and life-threatening complications of acute myocardial infarction. The aim of this study was to evaluate the early and long-term results of the patients after surgical repair of postinfarction VSD by infarct exclusion technique.

Methods
A total of 32 consecutive patients (mean age, 62.5 10.5 years) underwent postinfarction VSD repairusing a standardized technique in our department. A retrospective analysis of clinical and operative data, predictors of early mortality, and long-term survival was performed. The localization of VSD was posterior in 50% and anterior in 50% of the patients.

Results
The hospital mortality was 31.2% (10 patients). The most common cause of hospital death was persistent low cardiac output. The mortality of the posterior VSD group was significantly lower than that of the anterior VSD group (18.7% and 43.7%, respectively, p = 0.01). Intra-aortic balloon pump support and absence of cardiac shock were significantly associated with a lower risk of hospital mortality (p = 0.0001 and p = 0.0009, respectively). The actuarial survival rates of in-hospital survivors at 5 and 10 years were 79% 2% and 51% 3%, respectively.

Conclusions
The repair of postinfarction VSD by the infarct exclusion is feasible and safe. This techniqueseems to offer sufficient favorable early and long-term results compared with other techniques. Early indication, preoperative intra-aortic balloon pump support may improve the surgical results. Preoperative cardiogenic shock carries a poor prognosis for this patient group.

Postinfarction Ventricular Septal Defects: Towards a New Treatment Algorithm?

Simon Maltais MD, MS, Reda Ibrahim MD, Arsne-Joseph Basmadjian MD, Michel Carrier MD, Denis Bouchard MD, Raymond Cartier MD, Philippe Demers MD, Martin Ladouceur MS, Michel Pellerin MDand Louis P. Perrault MD, PhD, ,

Cardiac Surgery, Montreal Heart Institute and Universit de Montral, Montreal, Cardiology Department, Montreal Heart Institute and Universit de Montral, Montreal, Biostatistics Department, McGill University Health Centre, Montreal, Quebec, Canada Accepted 20 November 2008.

Background
We reviewed our experience at the Montreal Heart Institute with early surgical and percutaneous closure of postinfarction ventricular septal defects (VSD).

Methods
Between May 1995 and November 2007, 51 patients with postinfarction VSD were treated. Thirty-nine patients underwent operations, and 12 were treated with percutaneous closure of the VSD.

Results
Half of the patients were in systemic shock, and 88% were supported with an intraaortic balloon pump before the procedure. Before the procedure, 14% of patients underwent primary percutaneous transluminal coronary angioplasty. The mean left ventricular ejection fraction was 0.44 0.11, and mean Qp/Qs was 2.3 1. Time from acute myocardial infarction to VSD diagnosis was 5.4 5.1 days, and the mean delay from VSD diagnosis to treatment was 4.0 4.0 days. A moderate to large residual VSD was present in 10% of patients after correction. Early overall mortality was 33%. Residual VSD, time from myocardial infarction toVSD diagnosis, and time from VSD diagnosis to treatment were the strongest predictor of mortality. Twelve patients were treated with a percutaneous occluder device, and the hospital or 30-day mortality in this group was 42%.

Conclusion Small or medium VSDs can be treated definitively with a ventricular septal occluder or initially to stabilize patients and allow myocardial fibrosis, thus facilitating delayed subsequent surgical correction

Repair of post-infarct ventricular septal defect with or without coronary artery bypass grafting in the northwest of England: a 5-year multi-institutional experience
BARKER T. A. ; RAMNARINE I. R. ; WOO E. B. ; GRAYSON A. D.; AU J. ; FABRI B. M. ; BRIDGEWATER B. ; GROTTE G. J. ; (1) Department of Cardiothoracic Surgery, Manchester Royal Infirmary, Manchester, ROYAUME-UNI (2) Department of Cardiothoracic Surgery, The Cardiothoracic Centre-Liverpool, Thomas Drive, Liverpool, L14 3PE, ROYAUME-UNI (3) Department of Clinical Governance, The Cardiothoracic Centre-Liverpool, Thomas Drive, Liverpool, L14 3PE, ROYAUME-UNI (4) Department of Cardiothoracic Surgery, Blackpool Victoria Hospital, Blackpool, ROYAUME-UNI (5) Department of Cardiothoracic Surgery, Wythenshawe Hospital, Manchester, ROYAUME-UNI

Objective: To present the 5-year experience of the northwest of England's surgical repair of post myocardial infarction (MI) ventricular septal defects (VSD). Our primary aim was to evaluate the effect of concomitant coronary artery bypass grafting (CABG) on mid-term survival and also to identify prognostic indicators. Methods: A multi-centre regional observational study involving clinical data from 65 consecutive patients who underwent post MI VSD repair in the northwest of England between April 1997 and March 2002. Both prospective and retrospective collection of preoperative, operative and postoperative information was performed. Patient follow-up was performed by linking their records to the National Strategic Tracing Service database. Multivariate logistic regression and Cox proportional hazards analyses were used to identify independent risk factors for poor prognosis. Results: Of the 65 patients included in the study, 42 (64.6%) underwent concomitant CABG with a median of two grafts. The majority of patients who had their coronary arteries grafted had multivessel disease (92.9% Overall 30-day mortality was 23.1%. Predictors of poor prognosis included preoperative inotropes (P < 0.001) and total occlusion of infarct related artery (P = 0.03). The crude hazard ratio (HR) of mid-term mortality for concomitant CABG patients was 0.82 [95% confidence interval (CI) 0.38-1.78; P = 0.62]. After adjustment for differences in patient and disease characteristics, the adjusted HR of mid-term mortality for concomitant CABG patients was 0.17 (95% CI 0.04-0.74; P = 0.019). The adjusted freedom from death in the concomitant CABG patients at 30 days, 1, 2, and 4 years was 96.2%, 91.6%, 88.8%, and 82.8%, respectively, compared with 79.1%, 58.8%, 49.1%, and 32.2% for the non-concomitant CABG patients. Conclusion: These data provide evidence that concomitant CABG is significantly beneficial to mid-term mortality rates. We recommend that patients who present with post MI VSD who have multivessel disease should be routinely revascularised.

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