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An 81-year-old woman presented with dyspnea of 4 hours' duration associated with a systolic blood pressure of 180 mmHg. An electrocardiogram showed inferolateral ST-segment elevation and subtle PR-segment elevation in lead aVR (Fig. 1).

Fig. 1. Electrocardiogram shows sinus rhythm with frequent premature ventricular contractions, ST-segment elevation inferolaterally with a single Q wave in lead III, and PR-segment elevation in lead aVR.Fig. 1. Electrocardiogram shows sinus rhythm with frequent premature ventricular contractions, ST-segment elevation inferolaterally with a single Q wave in lead III, and PR-segment elevation in lead aVR.Fig. 1. Electrocardiogram shows sinus rhythm with frequent premature ventricular contractions, ST-segment elevation inferolaterally with a single Q wave in lead III, and PR-segment elevation in lead aVR.
Fig. 1 Electrocardiogram shows sinus rhythm with frequent premature ventricular contractions, ST-segment elevation inferolaterally with a single Q wave in lead III, and PR-segment elevation in lead aVR.

Citation: Texas Heart Institute Journal 43, 4; 10.14503/THIJ-15-5619

Results of emergency catheterization revealed occlusion of the distal right coronary artery. After being given a bolus of bivalirudin in preparation for percutaneous coronary intervention (PCI), the patient experienced cardiac arrest due to pulseless electrical activity. Spontaneous circulation returned after 10 minutes of cardiopulmonary resuscitation. Repeat angiography revealed slow flow in the right coronary artery (Fig. 2). Right-sided heart catheterization revealed an equalization of intracardiac filling pressures (22 mmHg) and an oxygenation step-up from the right atrium to the pulmonary artery (from 49% to 80% saturation). A surface echocardiogram showed a large pericardial effusion (Fig. 3). Emergency pericardiocentesis yielded 2.5 L of blood from the pericardial space. An intra-aortic balloon pump was placed for hemodynamic support.

Fig. 2. Coronary angiogram of the right coronary artery (left anterior oblique view) shows distal occlusion and evidence of slow flow.Fig. 2. Coronary angiogram of the right coronary artery (left anterior oblique view) shows distal occlusion and evidence of slow flow.Fig. 2. Coronary angiogram of the right coronary artery (left anterior oblique view) shows distal occlusion and evidence of slow flow.
Fig. 2 Coronary angiogram of the right coronary artery (left anterior oblique view) shows distal occlusion and evidence of slow flow.

Citation: Texas Heart Institute Journal 43, 4; 10.14503/THIJ-15-5619

Fig. 3. Transthoracic echocardiogram (subcostal view) shows a large anterior pericardial effusion (E) and the left ventricle (LV).Fig. 3. Transthoracic echocardiogram (subcostal view) shows a large anterior pericardial effusion (E) and the left ventricle (LV).Fig. 3. Transthoracic echocardiogram (subcostal view) shows a large anterior pericardial effusion (E) and the left ventricle (LV).
Fig. 3 Transthoracic echocardiogram (subcostal view) shows a large anterior pericardial effusion (E) and the left ventricle (LV).

Citation: Texas Heart Institute Journal 43, 4; 10.14503/THIJ-15-5619

A left ventriculogram showed ventricular double rupture involving the inferoposterior left ventricle and interventricular septum (Fig. 4). Operative repair was not feasible, and the patient died.

Fig. 4. A) Left ventriculogram (right anterior oblique view) shows a ventriculoseptal defect with left-to-right flow (asterisk) and extravasation into the pericardial space (P). B) Delayed-injection image shows further extravasation into the pericardial space (P). Also visible are a pericardial drain, an intra-aortic balloon pump, a pulmonary artery catheter, pacing pads, and an angled pigtail catheter. / Supplemental motion image is available for Figure 4.Fig. 4. A) Left ventriculogram (right anterior oblique view) shows a ventriculoseptal defect with left-to-right flow (asterisk) and extravasation into the pericardial space (P). B) Delayed-injection image shows further extravasation into the pericardial space (P). Also visible are a pericardial drain, an intra-aortic balloon pump, a pulmonary artery catheter, pacing pads, and an angled pigtail catheter. / Supplemental motion image is available for Figure 4.Fig. 4. A) Left ventriculogram (right anterior oblique view) shows a ventriculoseptal defect with left-to-right flow (asterisk) and extravasation into the pericardial space (P). B) Delayed-injection image shows further extravasation into the pericardial space (P). Also visible are a pericardial drain, an intra-aortic balloon pump, a pulmonary artery catheter, pacing pads, and an angled pigtail catheter. / Supplemental motion image is available for Figure 4.
Fig. 4 A) Left ventriculogram (right anterior oblique view) shows a ventriculoseptal defect with left-to-right flow (asterisk) and extravasation into the pericardial space (P). B) Delayed-injection image shows further extravasation into the pericardial space (P). Also visible are a pericardial drain, an intra-aortic balloon pump, a pulmonary artery catheter, pacing pads, and an angled pigtail catheter. Supplemental motion image is available for Figure 4.

Citation: Texas Heart Institute Journal 43, 4; 10.14503/THIJ-15-5619

Comment

Risk factors for myocardial rupture after myocardial infarction (MI) include hypertension, first infarction, and the absence of collateral coronary circulation.1 Combined rupture of the ventricular septum and left ventricular free wall, a form of ventricular double rupture, is a rare late presentation of acute MI. The authors of a single-center case series described ventricular double rupture in 0.3% of patients who presented with acute MI.2

In hospitalized patients who sustain cardiac rupture, the mortality rate remains elevated at 75%.3 In ventricular double rupture, survival is exceedingly rare despite surgical intervention.4

Our patient's clinical presentation was probably caused by impending ventricular double rupture and recurrent ischemia after an initially silent MI earlier in the week. Anticoagulation might have disrupted a pseudoaneurysm, causing tamponade. This case illustrates the importance of alertness for potential mechanical complications in patients who are undergoing primary PCI for ST-segment-elevation MI.

References

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    Wessler S,
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    The pathogenesis of spontaneous cardiac rupture. Circulation1952;6(
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  • 2.

    Tanaka K,
    Sato N,
    Yasutake M,
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    Ochi M,
    et al. Clinicopathological characteristics of 10 patients with rupture of both ventricular free wall and septum (double rupture) after acute myocardial infarction. J Nippon Med Sch2003;70(
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    ):21–7.

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    Figueras J,
    Alcalde O,
    Barrabes JA,
    Serra V,
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    Cortadellas J,
    Lidon RM.
    Changes in hospital mortality rates in 425 patients with acute ST-elevation myocardial infarction and cardiac rupture over a 30-year period. Circulation2008;118(
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    Successful surgical repair of ventricular double rupture. Can J Cardiol2011;27(
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Copyright: © 2016 by the Texas Heart® Institute, Houston
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Fig. 1
Fig. 1

Electrocardiogram shows sinus rhythm with frequent premature ventricular contractions, ST-segment elevation inferolaterally with a single Q wave in lead III, and PR-segment elevation in lead aVR.

Fig. 2
Fig. 2

Coronary angiogram of the right coronary artery (left anterior oblique view) shows distal occlusion and evidence of slow flow.

Fig. 3
Fig. 3

Transthoracic echocardiogram (subcostal view) shows a large anterior pericardial effusion (E) and the left ventricle (LV).

Fig. 4
Fig. 4

A) Left ventriculogram (right anterior oblique view) shows a ventriculoseptal defect with left-to-right flow (asterisk) and extravasation into the pericardial space (P). B) Delayed-injection image shows further extravasation into the pericardial space (P). Also visible are a pericardial drain, an intra-aortic balloon pump, a pulmonary artery catheter, pacing pads, and an angled pigtail catheter.

Supplemental motion image is available for Figure 4.

Contributor Notes

Section Editor: Raymond F. Stainback, MD, Department of Adult Cardiology, Texas Heart Institute, 6624 Fannin St., Suite 2480, Houston, TX 77030

From: Division of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215

Address for reprints: Colin T. Phillips, MD, Division of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215, E-mail: ctphilli@bidmc.harvard.edu