Surgical treatment of left ventricular wall rupture, regarded as a consequence of Takotsubo cardiomyopathy.

OBJECTIVE: We present the case of possible reverse type of TCM in a female patient presented with progressive left ventricular dysfunction and its rupture in pericardium.
METHODS: The detailed history, physical examination, laboratory tests, electrocardiography, serial echocardiography, coronary angiography with left ventriculography were performed to diagnose possible Takotsubo cardiomyopathy in 63-year old woman admitted to our center with complaints of dyspnea, lightheadedness, weakness and signs of hypotension and history of inferior myocardial infarction, acute left ventricular aneurysm, and effusive pericarditis and pleuritis, developed after emotional stress 5 months ago.
RESULTS: Clinical evaluation revealed unremarkable laboratory tests, normal troponin values, signs of old inferior myocardial infarction on electrocardiogram, and left ventricular (LV) dilatation and dysfunction, akinesia of LV infero-lateral wall with thinning and its rupture and blood shunting in pericardium. Her coronary angiography revealed normal coronary arteries. The diagnosis of pheochromocytoma was excluded. The patient underwent surgery under cardiopulmonary bypass with removal of LV pseudoaneurysm. The patient was discharged from hospital with improvement in NYHA class and LV function.
CONCLUSION: Thus, in female postmenopausal patients presenting with acute myocardial infarction signs complicated by pericarditis, intact coronary arteries and LV dysfunction with emotional stress as triggering factor, reverse type of TCM should be considered and proper management applied to prevent development of life-threatening complications like LV rupture.

Introduction

The stress cardiomyopathy or Takotsubo cardiomyopathy (TCM), described by Sato et al.,[1] is a transient left ventricular (LV) apical ballooning, accompanied by LV dysfunction.[2] Clinical manifestations of TCM resemble acute myocardial infarction (MI), although both may coexist,[3,4] and it usually develops in postmenopausal women with intact coronary arteries. Emotional stress with sympathetic activation and catecholamine’s cardiac toxicity is the underlying mechanism in most cases, though microvascular dysfunction, coronary spasm and inflammation contribute as well.[3] Usually, hypo-akinesia of apical and midventricular LV segments and hyperkinesia of basal segments are observed; however, the reverse (inverted) types were also described.[1,3-7] Reverse type accounted for 23.3% of all TCM cases and emotional stress was a leading triggering factor. The prognosis of TCM is usually benign; however, several cases of LV wall rupture were described.[3-9]

We present the case of reverse type of TCM in a female patient presented with progressive LV dysfunction and rupture of LV wall in pericardium.

Case report

A 63-year-old female patient was admitted with complaints of acute chest pain without irradiation lasting for 2 days, dyspnea, lightheadedness, weakness and signs of hypotension. She had had history of hypertension for past 10 years. She was admitted to cardiology department 5 months ago with chest pain and was treated with the diagnosis of acute inferior MI, acute LV aneurysm, New York Heart Association (NYHA) class 4 and effusive pericarditis and pleuritis. Analysis of her serial echocardiograms (echo) during previous hospitalization revealed progressive LV dilatation and dysfunction, with accumulation of pericardial fibrinous detachments and effusion during 14 days of follow-up. Her troponin values were equal to 0.0 ng/mL.

In our clinic, her laboratory tests were unremarkable. ECG showed signs of old inferior wall MI and lateral wall ST-T abnormalities (Figure 1(a)). Her echo displayed LV dilatation ((left ventricular end-diastolic dimension (LVEDD), 7.6 cm; left ventricular end-systolic dimension (LVESD), 6.0 cm)), reduced left ventricular ejection fraction (LVEF, 35%), moderate mitral regurgitation, hypo-akinesia and thinning (0.6 mm) of LV infero-lateral wall with rupture and cross-over blood shunt through two defects into pericardium (Figure 1(b) and (c)) and thrombi (Figure 1(d)). Coronary angiography and left ventriculography revealed intact coronary arteries and blood shunt from postero-basal segment into pericardium. She had no clinical or laboratory signs of pheochromocytoma, neither she had signs of myocarditis, recent cranial trauma or intracranial hemorrhage, and her echo ruled out hypertrophic cardiomyopathy.

Figure 1.

(a) ECG shows Q wave in leads III and AVF, negative T waves DII, DIII and AVF, and ST-T abnormalities in V5-V6. 2D and Color Doppler echo images of (b) akinesia, thinning and rupture of LV infero-lateral wall; (c) LV to pericardium cross-over blood shunt through defects; and (d) massive thrombosis of cavity and inferolateral wall.

The patient underwent surgery under cardiopulmonary bypass with resection of LV pseudoaneurysm and closure of left ventricular posterior wall (LVPW) defect. During operation, we revealed pulsating mass along LV postero-diaphragmatic wall (Figure 2(a)). Cardiolysis of LVPW was applied and the mass 1.5×1.0 cm of size with dense cover was partially relieved from adhesions. Removal of dense adhesions from LVPW exposed the aneurysmal sac and defect of 1 × 1 cm communicating with LV cavity. Its cavity was filled and LV walls were covered by densely organized and epithelialized tissue (Figure 2(b) and (c)). The defect was sutured on pericardial patch; free walls of sac were dissected and removed. Microscopic analysis of samples showed thickening, sclerosis, serous-fibrinous inflammation of inner wall and nonspecific inflammation of the outer wall of pericardium. The postoperative period was stable; patient was winded off the ventilation 16 h and mobilized 36 h after surgery. Her echo after operation (Figure 2(d)) revealed reduction in LV size (LVEDD, 6.2 cm and LVESD, 4.7 cm), increase in LVEF (46%) and mild mitral regurgitation. The patient was discharged from hospital.

Figure 2.

Intraoperative views of (a) pulsating mass 15–10 cm in size at postero-diaphragmatic wall of LV; (b, c) organized and epithelialized content of the aneurysmatic sac and LV wall; and (d) postoperative echo image of LV after resection of sac and repair of defect.

Discussion

Analyzing patient’s history, we suggest the first manifestation of the disease was 5 months ago, when after emotional stress she had experienced symptoms of acute MI complicated by LV aneurysm. Furthermore, due to deterioration of LV function and progressive dilatation of aneurysm with LV rupture after another emotional stress, she was admitted to our clinic. Taking into account female sex, postmenopausal state, history, echo, catheterization and intraoperative findings, intact coronary arteries, and the development of LV aneurysmatic dilatation after emotional stress, we can consider this case as an inverted type (reverse type) of TCM during her first admission according to Mayo clinic criteria[10,11] and later complicated by LV wall rupture and pericardial involvement when she was referred to our clinic for surgery. We do not exclude if she had had the inferior wall MI in the presence of intact coronary arteries.[4,12] Previous cases demonstrated inverted type with akinesia of antero-lateral diaphragmal, posterior and basal midportion walls without apical ballooning,[6,7] as well as myocardial rupture was described in the setting of TCM.[8,9] Our case is a rare reverse type of TCM with rupture of posterior, infero-lateral walls into pericardium. Thus, in female postmenopausal patients presenting with acute MI signs complicated by pericarditis, intact coronary arteries and LV dysfunction with emotional stress as triggering factor, reverse type of TCM should be considered and proper management applied to prevent development of life-threatening complications like LV rupture.