Daughter, You Broke My Heart

Abstract

We report the case of a 59-year-old trained runner, who sustained an acute myocardial infarction, with residual effort angina, following extreme exertion while experiencing severe anxiety. Coronary angiography revealed that this patient had a myocardial bridge at the mid-left anterior descending artery, and an occlusive clot had developed at the proximal end of the muscular bridge.

We discuss the possible relationships between the various circumstances of this sudden event. We argue that, under exceptional conditions, myocardial bridges can lead to myocardial infarction by clot formation.

Muscular or myocardial bridges (MBs) of the coronary arteries have been the object of numerous reports in the medical literature, in different contexts. Only a few reports have described specific details regarding the presentation of the occasional case of MB that becomes complicated by a severe clinical event. We present such evidence in the case of a patient who suffered an acute myocardial infarction, followed by residual angina pectoris.

Case Report

In April 2004, a 59-year-old man was referred to our institution because of recent-onset angina. His relevant medical history included surgical clipping of a cerebral aneurysm 1 year before the current presentation. At the same time, he was diagnosed as having hypertension and dyslipidemia, and was treated with angiotensin-converting enzyme inhibitors and fibrates. Cigarette smoking (82 packs per year) had been interrupted 3 years earlier. The patient had previously been an amateur marathon and a triathlon runner.

About 2 months before presentation, the patient had emergently rescued his 15-year-old daughter from a near-drowning accident in a river, while on vacation in the wilderness. During the event, he underwent extreme and unusual physical exertion, carrying her for 5 miles in his arms on a rugged mountain trail, while extremely frightened and anxious about his daughter's condition. (She was comatose, with profuse head-bleeding after suffering a fall.) During such extreme effort, he experienced intense, oppressive chest pain that radiated to his jaws, with shortness of breath and faintness. The symptoms resolved spontaneously, but only after 8 hours of rest. Nonetheless, the patient did not go to a doctor until a month later, with a history of effort-related chest pains, typical of angina pectoris. After another month of continuing symptoms, he was referred to our institution. We performed dobutamine echocardiography, which revealed baseline apical myocardial hypokinesia and stress-induced reversible worsening, with a resting ejection fraction of 0.60. On coronary angiography, total occlusion of the left anterior descending artery (LAD) distal to the 1st diagonal branch, but proximal to a MB, was observed (Fig. 1), with evidence of distal retrograde filling from the right coronary artery. The rest of the coronary circulation was normal. The left ventricular ejection fraction was 0.50, with mild apical hypokinesia. After successful proximal LAD balloon and stent angioplasty by use of a 3.0×28-mm paclitaxel-eluting stent, a MB distal to the occlusion became apparent. Intracoronary nitroglycerin administration led to marked worsening of the systolic narrowing (Fig. 2). Of note, the initial balloon inflation resulted in complete expansion of the balloon at low pressure (3 atm), which likely was evidence of a soft arterial occlusion, as might be caused by a fresh clot. When last evaluated, 6 months after the procedure, the patient was asymptomatic.

Fig. 1 Preoperative left coronary angiogram (right anterior oblique projection) shows A) total proximal occlusion of the left anterior descending artery; B) the appearance of the distal artery after a coronary guidewire (but not the balloon) was passed through the occlusion. Restoration of minimal patency of the vessel revealed the extent of the thrombotic obstruction (18 mm long), proximal to the muscular bridge.

Fig. 2 Postoperative A) diastolic and B) systolic left coronary angiographic images (left anterior oblique projection) after administration of 100 g intracoronary nitroglycerin. The stented proximal left anterior descending artery is followed by a segment (arrows) that appears normal in diastole but is severely obstructed in systole. C) Angiographic image in the right anterior oblique projection is shown in systole. Arrows indicate the obstructed segment.

Discussion

Muscular or myocardial bridge is defined as an anomalous course of a coronary artery, in which an epicardial vessel dips intramyocardially, with resulting compression during systole.^1–7 This circumstance has led to a proposal of the name “coronary underpass,” rather than MB.¹

The angiographic prevalence of MBs in the general population is between 0.15% and 25%.^1,2 This percentage increases to 40% after nitroglycerin administration.^3,4 Even in autopsy series, a wide range in the prevalence of MBs (15%–80%) has been reported.^4,5 The proximal LAD is the main site affected by MBs, occurring with a reported relative incidence of 46% of the MB cases.^2,8 The length of MBs can range from 10 to 50 mm.⁴

Myocardial bridges are clinically diagnosed by angiography or intravascular ultrasonography (IVUS).^1,6 No typical clinical presentation has been recognized, and most carriers are asymptomatic.¹ Typically, in the presence of the MB, no abnormalities are observed during stress testing, even though occasional abnormalities are discussed in individual case reports.2,4,9,10

On intracoronary Doppler IVUS imaging, the flow pattern at MBs has been found to be reversed in systole,^2,6,11 and the coronary reserve is mildly decreased.^8,11 The Doppler flow profile has an early diastolic acceleration followed by a steep deceleration, leading to a “spike and plateau” pattern.^1,8,11 Another typical finding on IVUS is an echolucent halo, also called a “half moon” sign, that seems to be an artifact of systolic compression by the exploring fiberoptic catheter at the MB.^1,11

Intravascular ultrasonography and necropsy studies have shown that up to 88% of the patients who have MBs eventually develop atherosclerotic plaque in the segment proximal to the MB.^1,11,12 The plaque development might be related to the sudden systolic flow deceleration and increased shear stress at this site.^12–14 On the other hand, MBs protect against atherosclerotic plaque formation at the MB level: in several observational IVUS and necropsy studies, no intimal thickening at the intramural segment has been found, even in the presence of diffuse coronary disease.2,5,6,11 Thrombus formation in MB-related arteries has occasionally been reported as the cause of a myocardial infarction or sudden cardiac death.1,4,8,14

In our patient, it is likely that extreme exertion under conditions of severe emotional distress resulted in high systolic compression of the MB at the time of adrenergic surge, possibly causing secondary sustained spasm^1,15 and, finally, in proximal clot formation. As we mentioned, the MB coronary segment itself was free of thrombus.

We consider the present case report important to the issue of clinical prognosis in MBs. Our patient was indeed able to perform increasing degrees of exertion without symptoms, until the thrombotic event occurred. It is surprising to note that sudden occlusion of the LAD resulted in only mild anterior hypokinesia, with secondary onset of effort-related angina; there was no massive infarction, as might be expected when a total sudden occlusion occurs in a large vessel during prolonged exertion. Gradual institution of the permanent occlusion may have occurred (possibly recurrent thrombus formation and spontaneous lysis), which has been described in experimental ischemic preconditioning.¹⁶