A 64-year-old woman is hospitalized due to an acute anterior wall myocardial infarction. She presented with a 24-hour history of persistent midsternal burning chest pain and was found to have complete occlusion of the mid-left anterior descending artery. Successful percutaneous coronary intervention was performed with placement of a bare metal stent. The patient's past medical history is significant for uncontrolled type 2 diabetes mellitus, hypertension, hyperlipidemia, and active smoking. She has a strong family history of diabetes, stroke, and coronary artery disease. On the fourth day of hospitalization, the patient develops acute-onset shortness of breath and confusion. Blood pressure is 72/40 mm Hg and heart rate is 120/min with regular rhythm. Physical examination shows cold clammy extremities and diaphoresis. There is jugular venous distension with the patient in a semirecumbent position. Bibasilar crackles are present on chest auscultation. A harsh, loud holosystolic murmur is present at the left sternal border with a palpable thrill. The abdomen is soft with some tenderness in the right upper quadrant. ECG shows sinus tachycardia with deep T wave inversion in leads V1 to V5. Which of the following is the most likely cause of this patient's deterioration?

Question

A 64-year-old woman is hospitalized due to an acute anterior wall myocardial infarction.  She presented with a 24-hour history of persistent midsternal burning chest pain and was found to have complete occlusion of the mid-left anterior descending artery.  Successful percutaneous coronary intervention was performed with placement of a bare metal stent.  The patient's past medical history is significant for uncontrolled type 2 diabetes mellitus, hypertension, hyperlipidemia, and active smoking.  She has a strong family history of diabetes, stroke, and coronary artery disease.  On the fourth day of hospitalization, the patient develops acute-onset shortness of breath and confusion.  Blood pressure is 72/40 mm Hg and heart rate is 120/min with regular rhythm.  Physical examination shows cold clammy extremities and diaphoresis.  There is jugular venous distension with the patient in a semirecumbent position.  Bibasilar crackles are present on chest auscultation.  A harsh, loud holosystolic murmur is present at the left sternal border with a palpable thrill.  The abdomen is soft with some tenderness in the right upper quadrant.  ECG shows sinus tachycardia with deep T wave inversion in leads V1 to V5.  Which of the following is the most likely cause of this patient's deterioration?

Quizplus · Accepted Answer

11ec25c8_d36b_d96b_bc81_a31760a21583_MD0003_00 A delay in coronary reperfusion ≥24 hours from symptom onset correlates with extensive myocardial death and increases the risk of a mechanical complication following acute myocardial infarction (MI). Interventricular septum rupture typically occurs 3- 5 days following a large MI involving the left anterior descending artery or right coronary artery. Communication between the left and right ventricle leads to increased pressure and volume load on the right ventricle and results in acute right-sided and left-sided heart failure. Patients develop acute cardiogenic shock (eg, pulmonary edema, hypotension, confusion due to poor organ perfusion), and demonstrate jugular venous distension and hepatomegaly due to liver congestion. In addition, blood flowing from the left to right ventricle creates a harsh holosystolic murmur with palpable thrill that can be appreciated at the left sternal border. The diagnosis of interventricular septum rupture can be confirmed by pulmonary artery catheterization detecting a left-to-right shunt with a step-up in oxygen saturation from the right atrium to right ventricle or by transthoracic echocardiography with visualization of the septal defect. (Choice A) Acute stent thrombosis causes coronary artery occlusion and presents with recurrent chest pain and ST elevation on ECG. This patient's ECG demonstrates T wave inversions in the precordial leads consistent with evolving changes of a recent anterior MI, but no ST elevation. (Choices B and C) Aortic dissection typically presents with sudden onset of tearing chest/back pain and can cause acute aortic regurgitation (early diastolic murmur). Aortic valve perforation can occur as a complication of aortic valve endocarditis and also leads to acute aortic regurgitation. This patient's systolic murmur is not consistent with aortic dissection or aortic valve perforation. (Choices D and F) Rupture of the left ventricular free wall typically occurs between 5 days and 2 weeks following a large MI. Patients develop pericardial tamponade due to hemopericardium leading to rapid decompensation and death. A systolic murmur with palpable thrill is not typical. (Choice E) Papillary muscle rupture leads to acute, severe mitral regurgitation and presents with sudden-onset hypotension, dyspnea, and pulmonary edema. Compared to interventricular septum rupture, the systolic murmur of acute mitral regurgitation is soft and there is no palpable thrill present. In addition, a left-anterior descending lesion (as in this patient) is more likely to cause septum rupture rather than papillary muscle rupture. Educational objective: Rupture of the interventricular septum typically occurs 3-5 days after an acute myocardial infarction and presents with sudden-onset cardiogenic shock with hypotension, biventricular failure, and a new harsh holosystolic murmur with palpable thrill at the left sternal border. References: Ventricular septal rupture complicating acute myocardial infarction: a contemporary review. (http://www.ncbi.nlm.nih.gov/pubmed/24970335) Relevance of delayed hospital admission on development of cardiac rupture during acute myocardial infarction: study in 225 patients with free wall, septal or papillary muscle rupture. (http://www.ncbi.nlm.nih.gov/pubmed/9669261)

A 64-Year-Old Woman Is Hospitalized Due to an Acute Anterior