**4.1 Echocardiography**

Transthoracic echocardiography (TTE) remains the cornerstone of the non-invasive assessment of PI-VSD (Kishon, 1993). TTE is indicated in any patient who presents with evidence of acutely impaired ventricular function or in unexplained hemodynamic deterioration suggests a mechanical complication following an acute myocardial infarction (Buda, 1991). Echocardiography has the benefit of being able to assess both left and right ventricular function, the presence of potentially co-existing and confounding valvular diseases – typically mitral regurgitation, and with color flow imaging it can be 100% specific and sensitive in diagnosing a PI-VSD. Despite the utility of TEE in the acute assessment of a deterioritating patient, a high index of suspicion is needed when looking for a PI-VSD as traditional echo windows might miss a small or apical defect. Large pericardial effusions might suggest an associated free wall rupture.

Post Myocardial Infarction Ventricular Septal Defect 33

from a practical standpoint it is hard to argue the clear benefits of defining the coronary anatomy prior to a surgical intervention aimed at treating a complication of coronary – particularly given the long-established importance of optimal or complete revascularization. Again, since these patients have already undergone catheterization as part of the initial management of their initial ischemic event the question whether to proceed with catheterization is rarely encountered. However, as many of the patients develop septal rupture several days (or weeks) after their initial acute coronary insult, it is hard to argue the need for repeat cardiac catheterization if the diagnosis is clear, particularly if the nuances of the coronary anatomy have recently been determined. Conversely, in less clear clinical situations, repeat catheterization might suggest an alternative, and potentially more likely, diagnosis such

Although the diagnosis is often made at the time of initial cardiac catheterization or echocardiography, occasionally a PI-VSD may be encountered during other diagnostic imaging. While patients might be too hemodynamically unstable or the presence of an intraaortic balloon pump (or other ferrous containing or non-MRI safe device) might preclude MRI, with the growing indications and utilization of MRI for operative planning, PI-VSD might be encountered. Patients with low ejection fractions, cardiomyopathies, or suspicion for unusual cardiac anatomy, might have MRI performed to assess for myocardial viability, fibrosis, or valvular pathology. In these patients a PI-VSD may be an unsuspected finding (Figure 3). Although there is little literature describing the utility of MRI in PI-VSDs, using concepts derived from the literature on congenital shunts and pathology, MRI might be of value in assisting in defining the extent of the defect, the shunt fraction, right ventricular function, and other associated pathophysiology (Didier, 1986). MRI might be of additive value in cases of questionable catheterization or echocardiographic studies or in assessing the post-operative patient in which a residual shunt is suspected. Nevertheless, MRI is, in

Fig. 3. Cardiac MRI demonstrating an apical defect. Gated cine images indicated a left to right shunt in which quantitative assessment can be used to determine the shunt fractions

as acute stent thrombosis or disruption of an already unstable plaque.

general, not considered a first-line imagining diagnostic tool.

**4.3 Magnetic Resonance Imaging** 

and size of the defect.

Fig. 2. Transesophageal echo, 4-chamber view, demonstration an apical VSD with from from the left ventricle (LV) to the right ventricle (RV). The left atrium (LA) is also shown to illustrate the typical relationship of the defect to the mitral valve.

#### **4.2 Cardiac catheterization**

Since patients who present with ECG and laboratory evidence of myocardial ischemia often undergo early cardiac catheterization with coronary angiography, this test often represents the initial study to suggest or confirm a diagnosis. Because the pathophysiology typically is associated with extensive and acute ischemia of a large territory of myocardium, it is not surprising that the findings at catheterization are often different than what would be expected for patients with a history of chronic coronary artery disease in which compensatory development of septal collaterals has had time to developed. During the acute presentation, the findings often suggest a complete occlusion of a large coronary artery in the setting of relatively minimal disease. Single vessel disease is found in 64% of patients and since the left anterior descending (LAD) artery is often the culprit vessel this explains why antero-apical septal VSDs are found in 60% of cases. Conversely, acute occlusions of a dominant right coronary or circumflex artery accounts for the remaining cases that occur in the posterior septum. Seven percent have concomitant double vessel disease, and 29% have triple vessel disease.

More importantly is that the cardiac catheterization might be the initial confirming diagnostic test. As mentioned above, quantitative assessment of oxygen step-offs, when performed, will demonstrate an increase in the partial pressure of oxygen (PaO2) between the right atrium and ventricle – diagnostic of the left to right shunt. Left ventricular contrast injections, although less likely to be performed in a deteriorating patient secondary to the concern that additional contrast might further injure an already compromised renal function, is critical in patients with a suspected PI-VSD. Contrast injected into the LV will cross the defect (left-right shunt) and enter into the pulmonary arterial tree. This "pulmonary arteriogram" is characteristic for a VSD (Figure 1, see above).

Despite what may be perceived as the obvious value of early catheterization, the value is debatable. Opponents of mandatory catheterization advocate that in a clinically deteriorating patient in whom the diagnosis is clear it delays surgical management, the dye load may worsen already impaired renal function, and some reports suggest that considering the patterns of coronary disease typically encountered that coronary revascularization is actually a risk factor for a poor outcome (Muehrcke DD , 1992). Despite these theoretically arguments,

Fig. 2. Transesophageal echo, 4-chamber view, demonstration an apical VSD with from from the left ventricle (LV) to the right ventricle (RV). The left atrium (LA) is also shown to

Since patients who present with ECG and laboratory evidence of myocardial ischemia often undergo early cardiac catheterization with coronary angiography, this test often represents the initial study to suggest or confirm a diagnosis. Because the pathophysiology typically is associated with extensive and acute ischemia of a large territory of myocardium, it is not surprising that the findings at catheterization are often different than what would be expected for patients with a history of chronic coronary artery disease in which compensatory development of septal collaterals has had time to developed. During the acute presentation, the findings often suggest a complete occlusion of a large coronary artery in the setting of relatively minimal disease. Single vessel disease is found in 64% of patients and since the left anterior descending (LAD) artery is often the culprit vessel this explains why antero-apical septal VSDs are found in 60% of cases. Conversely, acute occlusions of a dominant right coronary or circumflex artery accounts for the remaining cases that occur in the posterior septum. Seven percent have concomitant double vessel

More importantly is that the cardiac catheterization might be the initial confirming diagnostic test. As mentioned above, quantitative assessment of oxygen step-offs, when performed, will demonstrate an increase in the partial pressure of oxygen (PaO2) between the right atrium and ventricle – diagnostic of the left to right shunt. Left ventricular contrast injections, although less likely to be performed in a deteriorating patient secondary to the concern that additional contrast might further injure an already compromised renal function, is critical in patients with a suspected PI-VSD. Contrast injected into the LV will cross the defect (left-right shunt) and enter into the pulmonary arterial tree. This

Despite what may be perceived as the obvious value of early catheterization, the value is debatable. Opponents of mandatory catheterization advocate that in a clinically deteriorating patient in whom the diagnosis is clear it delays surgical management, the dye load may worsen already impaired renal function, and some reports suggest that considering the patterns of coronary disease typically encountered that coronary revascularization is actually a risk factor for a poor outcome (Muehrcke DD , 1992). Despite these theoretically arguments,

"pulmonary arteriogram" is characteristic for a VSD (Figure 1, see above).

illustrate the typical relationship of the defect to the mitral valve.

**4.2 Cardiac catheterization** 

disease, and 29% have triple vessel disease.

from a practical standpoint it is hard to argue the clear benefits of defining the coronary anatomy prior to a surgical intervention aimed at treating a complication of coronary – particularly given the long-established importance of optimal or complete revascularization. Again, since these patients have already undergone catheterization as part of the initial management of their initial ischemic event the question whether to proceed with catheterization is rarely encountered. However, as many of the patients develop septal rupture several days (or weeks) after their initial acute coronary insult, it is hard to argue the need for repeat cardiac catheterization if the diagnosis is clear, particularly if the nuances of the coronary anatomy have recently been determined. Conversely, in less clear clinical situations, repeat catheterization might suggest an alternative, and potentially more likely, diagnosis such as acute stent thrombosis or disruption of an already unstable plaque.

#### **4.3 Magnetic Resonance Imaging**

Although the diagnosis is often made at the time of initial cardiac catheterization or echocardiography, occasionally a PI-VSD may be encountered during other diagnostic imaging. While patients might be too hemodynamically unstable or the presence of an intraaortic balloon pump (or other ferrous containing or non-MRI safe device) might preclude MRI, with the growing indications and utilization of MRI for operative planning, PI-VSD might be encountered. Patients with low ejection fractions, cardiomyopathies, or suspicion for unusual cardiac anatomy, might have MRI performed to assess for myocardial viability, fibrosis, or valvular pathology. In these patients a PI-VSD may be an unsuspected finding (Figure 3). Although there is little literature describing the utility of MRI in PI-VSDs, using concepts derived from the literature on congenital shunts and pathology, MRI might be of value in assisting in defining the extent of the defect, the shunt fraction, right ventricular function, and other associated pathophysiology (Didier, 1986). MRI might be of additive value in cases of questionable catheterization or echocardiographic studies or in assessing the post-operative patient in which a residual shunt is suspected. Nevertheless, MRI is, in general, not considered a first-line imagining diagnostic tool.

Fig. 3. Cardiac MRI demonstrating an apical defect. Gated cine images indicated a left to right shunt in which quantitative assessment can be used to determine the shunt fractions and size of the defect.

Post Myocardial Infarction Ventricular Septal Defect 35

As soon as the diagnosis is made an intra-aortic balloon pump should be placed. Coronary augmentation will assist the ischemic and compromised myocardium, but more importantly it will unload the left ventricle and improve cardiac output, end-organ perfusion, and reduce pulmonary shunting and over-circulation. However, the physiologic improvements with IABP and other inotropic or vasoactive medications should only be viewed as transient

Although some advocate a strategy of delayed repair, this approach is rarely successful. The theory is to give the friable necrotic myocardium time (3-6 weeks) to fibrosis thereby allowing for an easier and more secure repair. The scarred tissue will better hold suture and less likely to tear apart and result in an early post-operative failure. This approach appears reasonable, but it is rare that patients remain stable or can be support during this time period. While guidelines for delayed surgical management are lacking, this might be an option in those who are hemodynamically/physiologically stable with a delayed presentation, have no or minimal signs of pulmonary hypertension or over-circulation, and have a stable fluid balance with good renal function. Unfortunately, such patients are rare and less than 5-10% of all PI-VSD patients will survive to allow for delayed repair. Such an approach may represent a "survival of the fittest" perspective in those with minimal shunting and with strict attention to medical comorbidities and nutrition a period of close watchful waiting may work. This approach may also be used to justify waiting in patients who have other severe comordities preclude intervention and would in theory require optimization prior to surgery. Nevertheless, it is hard to argue that any other problem would improve to the point of making surgery safer in the setting of worsening right ventricular heart failure – a problem that by itself is very difficult to treat both pre and post-operatively. Although, one can argue that in these patients, unless early surgical repair is clearly contraindicated, that their physiologic reserve combined to a minimal pathophysiologic insult predisposes to a good outcome regardless of whether an

The initial attempts at repairing PI-VSD followed a surgical approach similar to that for congenital VSDs – through a ventriculotomy in the right ventricular outflow track (RVOT) (Cooley, 1957). It was quickly appreciated the significant limitations of this approach. Firstly, in an already compromised right ventricle, the outflow tract incision only further reduced residual RV function. In addition, while suited for many common types congenital VSD's near the aortic valve, the RVOT incision offered poor exposure of defects that tended to be much further down the septum towards the apex. Most importantly, because the patch and suture line was on the RV side, the defect was still exposed to LV pressures and consequently was at increased risk for patch dehiscence, early recurrence, and extension of the defect. Pioneering work by animal studies by Heimbecker in 1968 advocated an approach to the VSD thru the left ventricle in the region of the culprit vessel through infarcted myocardium – i.e., anterior defects approached through the anterior wall while posterior defects through the inferior wall. These techniques addressed the deficiencies of a RVOT approach (Heimbecker, 1968). The benefits of these animal studies were subsequently

After the patient arrives in the operating room, the patient is routinely anesthetized and pharmacologically paralyzed. If not already in place, all patients should have arterial monitoring lines and a pulmonary artery (Swan-Ganz) catheter inserted. Pressures and

validated clinically within several years (Javid, 1972)(Buckley, 1971)

and allow for finishing the pre-operative assessment.

early or late repair is performed.

**8. Operative management** 

**8.1 General considerations** 
