BUMC Proceedings 1999;12:305-308 Chest pain ANNE PLUENNEKE, MD, ROBERT C. STOLER, MD, AND WILLIAM C. ROBERTS, MD From the Departments of Internal Med...
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BUMC Proceedings 1999;12:305-308

Chest pain ANNE PLUENNEKE, MD, ROBERT C. STOLER, MD, AND WILLIAM C. ROBERTS, MD From the Departments of Internal Medicine (Pluennecke) and Cardiology (Stoler) and the Baylor Cardiovascular Institute (Roberts), Baylor University Medical Center, Dallas, Texas. Corresponding author: William C. Roberts, MD, Baylor Cardiovascular Institute, 4 Roberts, 3500 Gaston Ave., Dallas, Texas 75246.

ANNE PLUENNEKE, MD: A 75-year-old white man came to the emergency room because of chest pain. Three days earlier, he had developed chest pain that radiated to his left shoulder and left arm and that was associated with dyspnea, nausea and vomiting, and diaphoresis, These symptoms continued periodically until he came to the hospital. On the morning of admission, he presented at his doctor's office with a heart rate of 32 beats per minute and electrocardiographic changes consistent with acute myocardial infarction (AMI). He was then sent to the emergency department. He was known to have systemic hypertension, hypercholesterolemia, and borderline diabetes mellitus. He had had a stroke at age 63 (1987) and a left-sided transient ischemic attack followed by a right carotid endarterectomy at age 71 (1995). Also, he had had prostate cancer and a transurethral resection. He smoked cigarettes for 25 years but quit at age 45 (1969). He was retired from work in a radiator shop and is married with 2 children. He had never used drugs or alcohol. There was no family history of early cardiovascular disease. His medications included lisinopril, 40 mg daily; hydrochlorothiazide, 25 mg daily; potassium chloride, 10 twice daily; terazosin hydrochloride, 2 mg daily; enteric-coated acetylsalicylic acid, 325 mg daily; nifedipine, 30 mg daily; timolol maleate ophthalmic solution, each eye daily; leuprolide acetate injection, every 90 days; and 1 aspirin daily. On presentation to the emergency department, he was awake, alert, and comfortable. His blood pressure was 92/48 mm Hg; heart rate, 58 beats per minute; respiratory rate, 16 breaths per minute, and he was afebrile. He weighed 84 kg (186 pounds) and was 183 cm (72 inches) tall. Oxygen saturation was 97% on room air. His neck veins were flat, and he had no carotid bruits. There were no precordial rubs or murmurs. A fourth heart sound was present. A few bibasilar rules were heard posteriorly on pulmonary examination. No abnormalities were observed on abdominal examination. There was no peripheral cyanosis, clubbing, or edema. The peripheral pulses were good. Neurologic examination disclosed no abnormalities. Serum sodium was 135 mEq/L; potassium, 3.7 mEq/L; chloride, 99 mEq/L; bicarbonate, 29 mEq/L; blood urea nitrogen, 37 mg/dL; creatinine, 1.5 mg/dL; glucose, 224 mg/dL; albumin, 3.3 g/dL; total bilirubin, 0.8 mg/dL; hemoglobin, 12.2 g/dL; hematocrit, 35%; mean corpuscular volume, 93 fL; white blood cells, 14.8 x 103/?L, with 84% neutrophils, 7% lymphocytes, and 9% monocytes; platelets, 216 x 103/?L; aspartate aminotransferase, 211 U/L; alanine aminotransferase, 66 U/L; alkaline phosphatase, 75 U/L; creatine kinase, 1340 U/L; and troponin, 36 mg/L. Total serum cholesterol was 137 mg/dL. The serum

triglycerides were 59 mg/dL. Electrocardiogram was consistent with inferior (posterior) wall AMI, with Q waves and ST segment elevation in leads II, III, and VF. ST segments in lead aVL were depressed. Leads V1 and V2 also had Q waves that appeared to be consistent with a previously healed myocardial infarction in the anterior wall. The patient was admitted to the coronary care unit in a hemodynamically stable condition. He was treated with heparin, aspirin, oxygen, and nitroglycerin. He was free of chest pain upon arrival to the coronary care unit. On hospital day 1, left-sided cardiac catheterization was performed: the left ventricular pressure was 90/13 mm Hg; inferior wall akinesis; anterolateral wall hypokinesis; and left ventricular ejection fraction, 45%. Coronary angiography disclosed the following degrees of diameter narrowing: left main, 30%; left anterior descending, 90% (mid); ramus intermedius, 90%; left circumflex, 90%; and right, 100%, with collaterals to the distal right from the left circumflex. A short run of atrial fibrillation occurred and resolved spontaneously. This was his only arrhythmia during hospitalization. On hospital day 2, he complained of mid back pain that was positional. He remained hemodynamically stable in sinus bradycardia. On day 3, while with his family in his room feeling well and laughing, he suddenly began “gasping for air.” He rapidly was ventilated with an ambu bag, and telemetry showed sinus tachycardia. His pulse was palpable. He was intubated, and good breath sounds were audible bilaterally. He then became pulseless. The heart rate decreased to about 40 beats per minute. Epinephrine/atropine, dopamine, and normal saline were administered to no avail. Pericardiocentesis yielded 35 mL of blood without functional improvement. Nearly an hour of cardiopulmonary resuscitation was fruitless. CASE DISCUSSION ROBERT C. STOLER, MD: This 75-year-old man presented with an inferior wall AMI and did not receive thrombolytic therapy. Cardiac catheterization disclosed multivessel coronary artery disease, and while awaiting coronary artery bypass surgery, the patient died suddenly an estimated 3 to 6 days after onset of the AMI. Pulseless electrical activity was noted during attempts at resuscitation, which was unsuccessful. While assessing the potential causes of the patient's demise, it will be helpful to keep in mind a brief differential diagnosis of possible reversible causes of pulseless electrical activity, which include hypovolemia, hypoxemia, cardiac tamponade, tension pneumothorax, acidosis, hypothermia, hyperkalemia, drug overdose, and pulmonary embolus. Sudden cardiac death occurring in the period immediately following AMI can be divided broadly into 2 categories: electrical or mechanical events. Electrical causes of sudden death include tachy- and bradyarrhythmias, while a mechanical source involves rupture of some segment of the myocardium. Ventricular tachyarrhythmias occur frequently in patients following AMI.Ventricular tachycardia is most concerning when it is sustained. Monomorphic ventricular tachycardia usually arises from a preexisting scar of the myocardium, whereas polymorphic ventricular tachycardia is most commonly a manifestation of myocardial ischemia. The prognosis of patients with ventricular tachycardia that occurs within 48 hours of an AMI is generally the

same as that of patients without ventricular arrhythmias (1). The occurrence of sustained ventricular tachycardia >48 hours post AMI is associated with increased mortality at 1 year (2). The incidence of ventricular tachycardia increases as the serum potassium falls below 4.5 mEq/L (3). The incidence of ventricular fibrillation is now decreasing and occurs in 48 hours after the onset of AMI) is considerably worse, with clearly increased mortality. Late ventricular fibrillation is associated with anterior location of the AMI, and sinus tachycardia or atrial fibrillation at presentation (2). Treatment of ventricular tachycardia and ventricular fibrillation starts with maintaining the potassium level >4.5 mEq/L and the magnesium level >2.0 mg/dL (5). Since the advent of the coronary care unit, lidocaine prophylaxis has not been shown to improve mortality (6). Prompt defibrillation/cardioversion and pharmacologic maintenance with lidocaine most commonly or intravenous amiodarone are cornerstones of therapy. Electrophysiologic study and implantable cardioverter defibrillator implantation are often warranted, particularly in patients with late ventricular tachycardia or ventricular defibrillation. Bradyarrhythmias are not infrequently seen in patients with AMI. Mobitz type I block (Wenckebach) is seen in 10% of cases, most commonly in the inferior location (7). This block usually lasts 150 U/L, also correlate with increased risk of cardiac rupture (14).

Being female does not appear to be an independent risk factor for free wall rupture. In total numbers, men rupture more, but the percentage of women who have an AMI and then rupture is higher than that of those who have an AMI without rupture (17–20, 23, 25). Systemic hypertension has not proved to be a risk factor for rupture (17–20, 25, 26). In fact, long-standing hypertension can lead to hypertrophy, which can be protective against rupture (14). The time course from onset of AMI to free wall rupture ranges from 1 to 21 days. It occurs most commonly between days 2 and 6, with a peak at 50 hours. Nearly a third of ruptures, however, occur within the first 24 hours (27). The key to diagnosing rupture is having a high index of suspicion. The definitive diagnosis is largely dependent on pericardiocentesis and echocardiography. The finding of gross blood in the pericardial sac strongly suggests rupture and the need for urgent surgery (28). References 1. Eldar M, Sievner Z, Goldbourt U, Reicher-Reiss N, Kaplinsky E, Behar S. Primary ventricular tachycardia in acute myocardial infarction: clinical characteristics and mortality. The SPRINT Study Group. Ann Intern Med 1992;117:31–36. 2. Kleiman RB, Miller JM, Buxton AE, Josephson ME, Marchlinski FE. Prognosis following sustained ventricular tachycardia occurring early after myocardial infarction. Am J Cardiol 1988;62:528–533. 3. Nordrehaug JE, Johannessen KA, von der Lippe G. Serum potassium concentration as a risk factor of ventricular arrhythmias early in acute myocardial infarction. Circulation 1985;71:654–659. 4. Antman EM, Berlin JA. Declining incidence of ventricular fibrillation in myocardial infarction. Implications for the prophylactic use of lidocaine. Circulation 1994;84:764–773. 5. Higham PD, Adams PC, Murray A, Campbell RW. Plasma potassium, serum magnesium and ventricular fibrillation: a prospective study. Q J Med 1993;86:609–617. 6. Hine LK, Laird N, Hewitt P, Chalmers TC. Meta-analytic evidence against prophylactic use of lidocaine in acute myocardial infarction. Arch Intern Med 1989;149:2694–2698. 7. Antman EM, Braunwald EB. Acute myocardial infarction. In Braunwald EB, ed. Heart Disease: A Textbook of Cardiovascular Medicine, 5th ed. Philadelphia: WB Saunders Co, 1997:1184. 8. Bhandari AK, Sager PT. Management of peri-infarctional ventricular arrhythmias and conduction disturbances. In Nacarrelli GV, ed. Cardiac Arrhythmias: A Practical Approach. Mt. Kisco, NY: Futura Publishing, 1991:283. 9. Reeder GS. Identification and treatment of complications of myocardial infarction. Mayo Clin Proc 1995;70:880–884. 10. Held AC, Cole PL, Lipton B, Gore JM, Antman EM, Hockman JS, Corrao J, Goldberg RJ, Alpert JS. Rupture of the interventricular septum complicating acute myocardial infarction: a multicenter analysis of clinical findings and outcome. Am Heart J 1988; 116:1330–1336. 11. Barbour DJ, Roberts WC. Rupture of a left ventricular papillary muscle during acute myocardial infarction: analysis of 22 necropsy patients. J Am Coll Cardiol 1986;8:558– 565.

12. Bulkley BH, Roberts WC. Steroid therapy during acute myocardial infarction. A cause of delayed healing and of ventricular aneurysm. Am J Med 1974;56:244–250. 13. Silverman HS, Pfeifer MP. Relation between use of anti-inflammatory agents and left ventricular free wall rupture during acute myocardial infarction. Am J Cardiol 1987; 59:363–364. 14. Pohjola-Sintonen S, Muller JE, Stone PH, Willich SN, Antman EM, Davis VG, Parker CB, Braunwald E. Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of Infarct Size. Am Heart J 1989;117:809–818. 15. Becker R, Charlesworth A, Wilcox R, Hampton J, Skene A, Gore J. Late thrombolysis accelerates the onset of cardiac rupture. Circulation 1994;90(suppl 1):563–. 16. Roberts WC. The floating heart or the heart too fat to sink: analysis of 55 necropsy patients. Am J Cardiol 1983;52:1286–1289. 17. Mann JM, Roberts WC. Rupture of the left ventricular free wall during acute myocardial infarction: analysis of 138 necropsy patients and comparison with 50 necropsy patients with acute myocardial infarction without rupture. Am J Cardiol 1988;62:847–859. 18. Reddy SG, Roberts WC. Frequency of rupture of the left ventricular free wall or ventricular septum among necropsy cases of fatal acute myocardial infarction since introduction of coronary care units. Am J Cardiol 1989;63:906–911. 19. Mann JM, Roberts WC. Acquired ventricular septal defect during acute myuocardial infarction: analysis of 38 unoperated necropsy patients and comparison with 50 unoperated necropsy patients without rupture. Am J Cardiol 1988;62:8–19. 20. Mann JM, Roberts WC. Cardiac morphologic observations after operative closure of acquired ventricular septal defect during acute myocardial infarction: analysis of 16 necropsy patients. Am J Cardiol 1987;60:981–987. 21. Saffitz JE, Fredrickson RC, Roberts WC. Relation of size of transmural acute myocardial infarct to mode of death, interval between infarction and death and frequency of coronary arterial thrombus. Am J Cardiol 1986;57:1249–1254. 22. Roberts WC. Rupture of the left ventricular free wall during acute myocardial infarction without hemopericardium. Am J Cardiol 1990;65:1033–1034. 23. Melchior T, Hildebrant P, Kober L, Jensen G, Torp-Pedersen C. Do diabetes mellitus and systemic hypertension predispose to left ventricular free wall rupture in acute myocardial infarction? Am J Cardiol 1997;80:1224–1225. 24. Honan MB, Harrell FE, Reimer KA, Califf RM, Mark DB, Pryor DB, Hlatky MA. Cardiac rupture, mortality and the timing of thrombolytic therapy: a meta-analysis. J Am Coll Cardiol 1990;16:359–367. 25. Purcaro A, Costantini C, Ciampani N, Mazzanti M, Silenzi C, Gili A, Belardinelli R, Astolfi D. Diagnostic criteria and management of subacute ventricular free wall rupture complicating acute myocardial infarction. Am J Cardiol 1997;80:397–409. 26. Dellborg M, Held P, Swedberg K, Vedin A. Rupture of the myocardium. Occurrence and risk factors. Br Heart J 1985;54:11–16. 27. Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993;22:720–726. 28. Zahger D, Milgalter E. Clinical problem-solving. A broken heart. N Engl J Med 1996;334:319–321.