MANAGEMENT ISSUES

Mitral regurgitation due to coronary heart disease is multifactorial and papillary muscledysfunctionorruptureisoneofthecauses.Otherreasonsaredysfunctional ventricular remodelling with increased sphericity and mitral annular dilatation due to ventricular enlargement. Medical management includes vasodilators along with a diuretic, provided the blood pressure allows their use. In surgical treatment, since the valvular anatomy is generally not distorted, mitral valve replacement is not the answer. Instead restrictive annuloplasty, which involves insertion of an undersized ring to improve leaflet apposition, is preferable. Moreover, annuloplasty preserves left ventricular geometry and spares the patient from the problems of anticoagulation (thrombosis, bleeding and monitoring).

A 68-year old man came with his son to his treating cardiologist, for a periodic heart check-up. Three months back, the patient has sustained an anterior wall myocardial infarction (MI), for which he was treated in this very hospital. At that time, he received oral aspirin, sub-cutaneous enoxaparin and an infusion of nitroglycerine. He was not given thrombolytic therapy because he presented over 24 hours after the onset of his chest pain and Q waves had already appeared on the ECG. The patient also declined coronary angiography, because he was not ready to undergo a revascularization procedure. Thereafter, he did not develop post-MI angina, but he did complain of some fatigue and exertional breathlessness.

On examination, the patient was tachypneic while lying on the couch in the doctor’s chamber. The pulse rate was 96 beats/min. with a BP of 110/74 mm Hg over the right arm. The JVP was not raised and there was no edema over the ankles. The precordium was remarkable because of a prominent bulge and a double apical impulse. The apex beat was diffuse and sustained and extended medially and upwards, upto the 3rd intercostal space. On auscultation, the S1 and S2 were normal but a soft S3 sound was audible in early diastole. No murmur or pericardial friction rub was appreciated. The breath sounds were vesicular with few crepitations audible over the lower lung fields.

ECG showed attenuation of R waves in the antero-septal precordial leads. There was coving and elevation of the S-T segment with inversion of the T waves (Fig. 50.1). The cardiac Troponin -T test was negative. X-ray chest findings were increased cardio-thoracic ratio with a large bulge on the left border of the heart. An arc-like hemispherical calcification was seen within the bulge (Fig. 50.2).

ECHO revealed a dilated left ventricle with an ejection fraction of 35%. There was a large dyskinetic area involving the mid and distal interventricular septum as well as the left ventricular apex. The dyskinetic area underwent outward systolic expansion with a persistent deformity during diastole. The wall of the dyskinetic area was more echogenic than the adjacent myocardium. A laminated mass was observed contiguous with the dyskinetic area, with which it moved synchronously (Fig. 50.3). These findings are consistent with the diagnosis of left ventricular aneurysm with mural thrombus.

Figure 50.1: ECG showing R wave attenuation,

S-T coving and T wave inversion

Figure 50.2: X-ray showing an arc-like calcification within a ventricular bulge

Figure 50.3: ECHO showing a mural thrombus arising from the ventricular apex

CLINICAL DISCUSSION

A ventricular aneurysm usually develops after an anterior wall myocardial infarction, due to occlusion of the left anterior descending coronary artery. It rarely follows inferior wall infarction. On ECG, if the typical pattern of evolved myocardial infarction (MI) persists for three or more months after acute MI, ventricular aneurysm should be suspected. On precordial inspection, the ventricular aneurysm produces a double left ventricular apical impulse. If the aneurysm is particularly large, it causes a sustained and diffuse apical impulse that extends medially and upwards, by two or more intercostal spaces.

A ventricular aneurysm is a large bulge-like deformity with a wide neck, located at or near the apex of the left ventricle. It is more common after damage to the anterior wall than after inferior wall infarction. The aneurysm exhibits dyskinesia or outward systolic expansion and a persistent deformity during diastole. The wall of the aneurysm is made of myocardium and is more echogenic than adjacent areas because it is made of fibrous scar tissue. It does not rupture but is often associated with a pedunculated or laminated ventricular thrombus.

A false aneurysm (pseudo-aneurysm) follows rupture of the left ventricular free wall, where the resultant hemopericardium clots and seals the breach by pericardial adhesions. The neck of the pseudo-aneurysm that communicates with the left ventricle is narrower than the aneurysm itself. The pseudo-aneurysm appears as a globular extracardiac pouch. A false aneurysm is located on the posterolateral LV wall and is more common after inferior wall than after anterior wall infarction. It is not expansile and remains constant in size. The wall of the aneurysm is made of pericardium and it is less echogenic than adjacent areas. It is friable, more liable to rupture and it is often filled with a thrombus caused by hemopericardium. The differences between a true aneurysm and a pseudoaneurysm are given in Table 50.1.

The development of a left ventricular aneurysm after acute myocardial infarction is a serious complication. Most patients go on to develop intractable congestive heart failure requiring aggressive decongestive therapy. There is a higher likelihood of ventricular tachycardia originating from the myocardial scar. The incidence of post-infarction unstable angina is also increased. Moreover, fragments of the mural thrombus in the aneurysmal pouch may dislodge to produce distal embolism (Table 50.2).

Table 50.2: Complications of ventricular aneurysm

•  Recurrent ventricular tachycardia •  Post-MI unstable angina pectoris •  Intractable congestive heart failure

•  Mural thrombus with distal embolism

MANAGEMENT ISSUES

Presence of a thrombus within a ventricular aneurysm is an established indication for oral anticoagulant therapy. Other definite indications for anticoagulation are mechanical prosthetic valve and left atrial thrombus with mitral stenosis. While it takes 3 to 5 days for the therapeutic effect of an oral anticoagulant like warfarin to take over, heparin is given in this interim period. Unfractionated heparin requires monitoring of prothrombin time (PT) and aPTT, but it is cost-effective. Low molecular weight heparin (LMWH) like enoxaparin is more expensive but does not require monitoring.

It is established practice to prescribe aspirin, a statin, an ACE-inhibitor and a beta-blocker to every survivor of myocardial infarction, unless there is a specific contraindication. A diuretic is added to reduce cardiac workload, if there are symptoms of pulmonary congestion. An aldosterone antagonist like spironolactone or eplerenone can reduce cardiac workload and improve ventricular remodelling. A nitrate is prescribed for post-infarction angina while amiodarone is used if serious ventricular arrhythmias are documented.

It is not uncommon for patients who develop a ventricular aneurysm, to have left main or triple-vessel coronary artery disease (TVD). Resection of the aneurysm can be contemplated at the time of coronary artery bypass grafting (CABG) surgery which is performed for either unstable angina or for refractory heart failure.