Correspondence
Clinical Problem-Solving: A Broken Heart
N Engl J Med 1996; 334:1474-1476May 30, 1996
- Article
To the Editor:
In their excellent commentary in the Clinical Problem-Solving article “A Broken Heart” (Feb. 1 issue),1 Drs. Zahger and Milgalter describe the difficulties in diagnosing subacute ventricular-wall rupture after myocardial infarction. Occasionally, color-flow mapping can be used to identify the rupture site noninvasively; we describe one such case.
A 67-year-old man was brought to the emergency department after collapsing in his bathroom. On regaining consciousness after 10 minutes, he reported severe chest pain. On arrival he had tachycardia and hypotension with clear lung fields and no jugular venous distention. He had a history of type II diabetes and hypertension. Three days before admission he had first experienced vague substernal pain, lasting several hours. Electrocardiography showed broad Q waves in leads I and aVL with inverted T waves in leads I, aVL, and V6, suggesting a lateral myocardial infarction.
Because of hemodynamic instability, echocardiography was performed. Two-dimensional echocardiography showed a normal-sized left ventricle. A large, localized pericardial effusion was seen around the left-sided chambers, compressing the left atrium (Figure 1AFigure 1
Two-Dimensional (Panel A) and Color-Flow (Panel B) Echocardiograms in a Patient with Chest Pain.). The basal segment of the posterolateral wall was dyskinetic. At the apical border of this infarcted zone, an area of echocardiographic “dropout” (accentuated during systole) suggested the presence of a myocardial tear (Figure 1A). Color-flow mapping showed a brief systolic transmural flow signal at this site, proving the occurrence of myocardial rupture (Figure 1B).The patient was taken to the operating room immediately. Intraoperatively, a localized pericardial hematoma due to adhesions from a previous episode of pericarditis was found to be covering a myocardial tear, which was closed with a patch. After an uneventful course, the patient left the hospital two weeks later.
Hemodynamic instability in a patient with a myocardial infarct mandates an echocardiogram. Under certain circumstances, imaging alone without pericardiocentesis may establish the diagnosis of a “broken heart.”
1 ReferencesC. Punzengruber, M.D.
C.-K. Ng, M.D.
General Hospital, Wels, A-4600 Austria1
Zahger D ,Milgalter E . A broken heart. N Engl J Med 1996;334:319-321
Full Text | Web of Science | Medline
To the Editor:
“A Broken Heart” is marred by a surprising reiteration of a long-discredited myth. The authors comment that “there are Q waves in I and aVL, suggesting a transmural infarction.” Q waves do not suggest anything of the kind, and never have. This long-lived misconception arose from an error in a study by Prinzmetal and associates in 1954.1 Using needle electrodes in infarcted canine hearts, they thought they had demonstrated that the subendocardium was electrically “silent” and did not contribute to the forces of depolarization — from which they concluded that only transmural infarcts could produce Q waves.
Several years later, they acknowledged error in the placement of the needle electrodes and withdrew their findings.2 The subendocardium, they found, was actively involved in depolarization; they pointed out that there was no reason in theory or in fact to suppose that subendocardial infarcts could not generate Q waves. Subsequent studies demonstrated that the presence or absence of Q waves did not distinguish transmural from subendocardial infarcts. About 50 percent of subendocardial infarcts are accompanied by pathologic Q waves, whereas 50 percent of transmural infarcts are not. The association is random.
In the case described in the Clinical Problem-Solving article, the infarct was obviously transmural, but the Q waves did not suggest the diagnosis — the hemorrhagic tamponade did. Non–Q-wave infarcts are just as likely to be transmural as the Q-wave variety and, by the same token, are just as likely to rupture.
2 ReferencesBrendan Phibbs, M.D.
Kino Community Hospital, Tucson, AZ 857131
Prinzmetal M ,Shaw CM Jr ,Maxwell MH , et al. Studies on the mechanism of ventricular activity. VI. The depolarization complex in pure subendocardial infarction: role of the subendocardial region in the normal electrocardiogram. Am J Med 1954;16:469-489
CrossRef | Web of Science | Medline2
Pipberger H ,Schwartz L ,Massumi RA ,Weiner SM ,Prinzmetal M . Studies on the mechanism of ventricular activity. XXI. The origin of the depolarization complex with clinical applications. Am Heart J 1957;54:511-530
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To the Editor:
In “A Broken Heart,” neither the authors nor the expert physician mentioned anything about the presence or absence of electrical alternans and low voltage on the patient's electrocardiogram. The triad of electrical alternans, low voltage, and tachycardia is a highly specific (though not a sensitive) indicator of cardiac tamponade.1 This might be a clue to the presence of cardiac tamponade in the appropriate clinical setting.
1 ReferencesKeivan Edalat, M.D.
Medical Center of Central Massachusetts, Worcester, MA 01605To the Editor:
The inspiratory fall in blood pressure from 70/40 to 55/35 mm Hg in the case of cardiac tamponade due to cardiac rupture described in “A Broken Heart” was present before mechanical ventilation was begun. However, the statement that pulsus paradoxus may be produced by positive-pressure respiration should be corrected. Positive-pressure respiration usually produces an inspiratory increase in systemic arterial systolic and pulse pressure, not a decrease. Massumi et al.1 used the term “reversed pulsus paradoxus” to describe this phenomenon. The inspiratory increase in arterial pressure is explained by both a transmission of positive intrathoracic pressure to the heart and great vessels and increased left ventricular preload.2 Thus, positive-pressure breathing may interfere with the recognition of true pulsus paradoxus in patients with cardiac tamponade.
2 ReferencesNoble O. Fowler, M.D.
University of Cincinnati Medical Center, Cincinnati, OH 45267-05421
Massumi RA ,Mason DT ,Vera Z ,Zelis R ,Otero J ,Amsterdam EA . Reversed pulsus paradoxus. N Engl J Med 1973;289:1272-1275
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Jardin F ,Farcot J-C ,Gueret P ,Prost J-F ,Ozier Y ,Bourdarias JP . Cyclic changes in arterial pulse during respiratory support. Circulation 1983;68:266-274
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Author/Editor Response
The authors and a colleague reply:
To the Editor: We thank Drs. Punzengruber and Ng for their excellent description of the identification of a myocardial tear in a patient by two-dimensional echocardiography and color-flow mapping. We saw a similar patient, who presented after a brief syncopal episode and had electrocardiographic findings suggestive of a recent (“silent”) myocardial infarction. Two-dimensional echocardiography revealed a small pericardial effusion and a basal posterior-wall segment that was thin and dyskinetic. A true myocardial tear in this area was thereafter diagnosed by angiography and confirmed during surgery. We agree with Drs. Punzengruber and Ng that the echocardiographic findings of pericardial effusion with a distinct dyskinetic wall segment in the setting of hemodynamic collapse and myocardial infarction are highly suggestive of myocardial rupture. However, the demonstration of transmural flow in such cases by Doppler techniques, as illustrated, appears to be extremely rare.
The comments of Drs. Phibbs and Fowler are well taken. Q waves cannot, of course, serve to diagnose transmural infarction with any certainty. Positive-pressure ventilation may indeed cause “reversed” pulsus paradoxus, and it would have been more appropriate to state that marked fluctuations of the blood pressure with respiration may be seen with mechanical ventilation.
Dr. Edalat reminds us of the classic triad of electrical alternans, low voltage, and tachycardia, which is specific for pericardial tamponade. As he correctly points out, this combination is not sensitive and our patient did not have either electrical alternans or low voltage on electrocardiography.
Doron Zahger, M.D.
Arthur Pollak, M.D.
Eliyahu Milgalter, M.D.
Hadassah Medical Center, Jerusalem 91240, Israel
