Cardiol Res

Cardiology Research, ISSN 1923-2829 print, 1923-2837 online, Open Access

Article copyright, the authors; Journal compilation copyright, Cardiol Res and Elmer Press Inc

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Case Report

Volume 9, Number 4, August 2018, pages 244-249

Takotsubo Cardiomyopathy-Induced Cardiac Free Wall Rupture: A Case Report and Review of Literature

Figure 1. Left ventriculogram showing the characteristic apical ballooning of TCM with moderate to severe mitral regurgitation.

Figure 2. Normal sections of the left anterior descending coronary artery without atherosclerotic stenosis or plaque rupture.

Figure 3. Mid-ventricular and apical cut sections of the heart showing an area of transmural hemorrhage with an apical slit-like rupture (black arrow).

Figure 4. Histopathology slides at the rupture site showing areas of hemorrhagic foci with polymorphnuclear cells infiltrates between the cardiac myocytes and hypereosinophilic contraction band necrosis (black arrow).

**Table 1.** The Demographic, Clinical, Electrocardiographic and Pathologic Features of the Reviewed Cases Along With the Reported Time Interval From Admission to the Occurrence of Cardiac Free Wall Rupture
Study	Age (Y)	Gender	EKG findings	Pathology findings	Interval to rupture
Akashi et al [22]	70	F	STE in leads I, II, III, aVL, aVF, V2 - V6. Pathologic Q waves were present in leads V1 - V5	Not done	75 h
Ishida et al [27]	67	F	STE in leads I, aVL, and V2 - V5 without reciprocal ST depression	Not done	7 days
Ohara et al [20]	79	F	STE in leads I, aVL and V1 - V5, depression in leads III and aVF, and abnormal Q wave in leads V1 - V4	Rupture in the anterior portion of the LV. Microscopically, inflammatory infiltrates and myocyte necrosis was evident at the site of the rupture with normal surrounding myocardial tissue	7 days
Mafrici et al [28]	87	F	STE in the inferior and V2 - V6 leads	Not done	1 day
Yamada et al [29]	71	F	STE in leads V4 - V6 and abnormal Q waves in leads V4 - V5	Not done	16 h
Sacha et al [24]	81	F	STE in leads I, II, III, aVL, aVF, V2 - V6	10 mm apical LV free wall rupture. Microscopically, transmural necrosis with hemorrhage and mild focal PMNL infiltration at the rupture site. Around the rupture, there were multiple fused foci of coagulation necrosis in various phase of myodestruction with contraction band necrosis	44 h
Shinozaki et al [19]	90	F	STE in leads I, aVL and V1 - V4	Not done	8 days
Stollberger et al [30]	71	F	STE and Q waves in leads II, III, aVF, V5 - V6	5 mm LV rupture in the apico-posterior region	4 h
Tsunoda et al [31]	74	F	STE in leads I, aVL, and V3 - V6; ST-depression in leads II, III, aVF; and R-wave diminishment in leads V3 and V4	11mm rupture at the anterior LV wall 30 mm above the apex and a small mural thrombus inside the necrotic wall. Microscopically, there were inflammatory cell infiltrations, interstitial fibrosis, hemorrhage, and coagulation necrosis without evidence of contraction band necrosis	10 days
Kurisu et al [18]	81	F	STE in leads I, II, III, aVF and V2 - V6	Not done	64 h
Mendiguchia et al [32]	69	F	STE in the anterolateral leads	Not done	2 days
Jagszewski et al [23]	82	F	STE in leads V1 - V5	Wide penetrating apical rupture. Microscopically, there were hypertrophied and disarrayed cardiomyocytes, surrounded by predominantly mononuclear inflammatory infiltrate and loose connective tissue as well the foci of hemorrhage	5 days
Kumar et al [21]	62	F	STE in leads I, II, V5 - V6	Slit-like transmural rupture at the midportion of the posterior ventricular wall with overlying epicardial hemorrhage. Microscopically, there were necrotic fibers with increased eosinophilic staining, contraction band necrosis, along with PMNL infiltration and bundles of wavy myocardial fibers	8 h
Hassan et al [26]	73	M	STE and Q waves in the inferior leads and ST depression over the anterolateral leads	1.2 cm perforation at the infero-basal region	Not reported
Indorato et al [25]	70	F	Not reported	0.4 cm apical rupture with hemorrhagic infarction extending from the anterior to posterior wall of LV. Microscopically, there were neutrophilic infiltration with small areas of spotty necrosis, hemorrhagic changes and a form of catecholaminergic myocarditis	4 h

Table 1. The Demographic, Clinical, Electrocardiographic and Pathologic Features of the Reviewed Cases Along With the Reported Time Interval From Admission to the Occurrence of Cardiac Free Wall Rupture

Study

Age (Y)

Gender

EKG findings

Pathology findings

Interval to rupture

Akashi et al [22]

STE in leads I, II, III, aVL, aVF, V2 - V6. Pathologic Q waves were present in leads V1 - V5

Not done

75 h

Ishida et al [27]

STE in leads I, aVL, and V2 - V5 without reciprocal ST depression

Not done

7 days

Ohara et al [20]

STE in leads I, aVL and V1 - V5, depression in leads III and aVF, and abnormal Q wave in leads V1 - V4

Rupture in the anterior portion of the LV. Microscopically, inflammatory infiltrates and myocyte necrosis was evident at the site of the rupture with normal surrounding myocardial tissue

7 days

Mafrici et al [28]

STE in the inferior and V2 - V6 leads

Not done

1 day

Yamada et al [29]

STE in leads V4 - V6 and abnormal Q waves in leads V4 - V5

Not done

16 h

Sacha et al [24]

STE in leads I, II, III, aVL, aVF, V2 - V6

10 mm apical LV free wall rupture. Microscopically, transmural necrosis with hemorrhage and mild focal PMNL infiltration at the rupture site. Around the rupture, there were multiple fused foci of coagulation necrosis in various phase of myodestruction with contraction band necrosis

44 h

Shinozaki et al [19]

STE in leads I, aVL and V1 - V4

Not done

8 days

Stollberger et al [30]

STE and Q waves in leads II, III, aVF, V5 - V6

5 mm LV rupture in the apico-posterior region

4 h

Tsunoda et al [31]

STE in leads I, aVL, and V3 - V6; ST-depression in leads II, III, aVF; and R-wave diminishment in leads V3 and V4

11mm rupture at the anterior LV wall 30 mm above the apex and a small mural thrombus inside the necrotic wall. Microscopically, there were inflammatory cell infiltrations, interstitial fibrosis, hemorrhage, and coagulation necrosis without evidence of contraction band necrosis

10 days

Kurisu et al [18]

STE in leads I, II, III, aVF and V2 - V6

Not done

64 h

Mendiguchia et al [32]

STE in the anterolateral leads

Not done

2 days

Jagszewski et al [23]

STE in leads V1 - V5

Wide penetrating apical rupture. Microscopically, there were hypertrophied and disarrayed cardiomyocytes, surrounded by predominantly mononuclear inflammatory infiltrate and loose connective tissue as well the foci of hemorrhage

5 days

Kumar et al [21]

STE in leads I, II, V5 - V6

Slit-like transmural rupture at the midportion of the posterior ventricular wall with overlying epicardial hemorrhage. Microscopically, there were necrotic fibers with increased eosinophilic staining, contraction band necrosis, along with PMNL infiltration and bundles of wavy myocardial fibers

8 h

Hassan et al [26]

STE and Q waves in the inferior leads and ST depression over the anterolateral leads

1.2 cm perforation at the infero-basal region

Not reported

Indorato et al [25]

Not reported

0.4 cm apical rupture with hemorrhagic infarction extending from the anterior to posterior wall of LV. Microscopically, there were neutrophilic infiltration with small areas of spotty necrosis, hemorrhagic changes and a form of catecholaminergic myocarditis

4 h