Clinical Images

Milking-Like Effect Secondary to Systolic Expansion of a Post-Infarction Left Ventricular Aneurysm

Ra√∫l Moreno, MD, FESC, Jes√∫s Perez del Todo, MD, Carlos Macaya, MD, FESC
Ra√∫l Moreno, MD, FESC, Jes√∫s Perez del Todo, MD, Carlos Macaya, MD, FESC
Systolic compression (milking) of the coronary arteries is almost always due to the existence of myocardial bridging. The prevalence of myocardial bridging ranges from 0.5% to 16% of patients submitted to coronary angiography, and is usually located at the proximal or mid segment of the left anterior descending coronary artery (LAD).1–3 Ocassionally, systolic compression may be caused by a systolic expansion of a left ventricular aneurysm.4 We present a patient with a post-infarction left ventricular aneurysm in whom coronary angiography showed a milking-like effect with systolic compression of the distal LAD. Case Report. A 81-year-old women with an acute anterior myocardial infarction successfully treated with thrombolysis was referred to cardiac catheterization because of cardiac failure requiring intravenous administration of inotropic drugs. Coronary angiography showed triple vessel disease with a severe lesion at the proximal LAD, that was subsequently treated with coronary stent implantation. Percutaneous coronary intervention was angiographically successful (Thrombolysis In Myocardial Infarction flow grade 3), although with a myocardial blush flow grade 0, indicating failure of myocardial reperfusion. Left ventriculography at this moment showed akinesia of anterior and lateral wall of the left ventricle. Six months later, the patient was referred to a new cardiac catheterization because of the presence of cardiac failure, in order to rule out in-stent restenosis. Coronary angiography showed absence of restenosis of the previously implanted coronary stent, a moderate narrowing distal to the stented site, and a distal systolic compression of the LAD (Figures 1 and 2). At ventriculography, left ventricle was dilated and had a severely depressed ejection fraction (0.20). A dyskinetic anterior wall of the left ventricle was shown, thus revealing systolic expansion of the left ventricle aneurysm, and not systolic contraction at a myocardial brigding, as the potential cause of external compresion of the distal LAD. The previous coronary angiography was reviewed, showing the absence of this systolic compression of LAD immediately after coronary stent implantation; in both studies, i.c. nitroglycerin (0.2 mg) was given. On the other hand, there was no collateral circulation to the vessel that could have contributed to the angiographic image at the distal LAD. Discussion. Systolic compression (milking) of coronary arteries is almost always due to the existence of segments that penetrate the myocardial tissue and are surrounded by muscular fibers (intramyocardial bridging). The prevalence of this finding ranges from 0.5% to 16% of patients submitted to coronary angiography, and from 15–85% in post-mortem studies.1,2,5 This prevalence may be higher in patients with left ventricular hypertrophy, especially in those with hypertrophic cardiomyopathy.6 Myocardial bridging is usually a benign condition with excellent long-term outcome, but it may be associated with myocardial ischemia, that may present as silent ischemia, angina, myocardial infarction, conduction disturbances, or even sudden cardiac death.3,7 In our patient, systolic compression of left anterior descending at angiography was not due to systolic contraction of myocardium through an intramural course of the artery, but to systolic expansion of an aneurysm. This could explain the distal location of this milking-like effect, since myocardial bridges are usually located at the proximal and middle portions of this vessel. Although sometimes the existence of milking may be evident only after restoration of coronary blood flow with coronary stenting,8 in our patient coronary angiography after stent implantation showed no systolic compression of the distal LAD. Some cases of myocardial brigding complicated by myocardial infarction have been reported.9 However, in our patient, anterior myocardial infarction was secondary to a proximal occlusion at the left anterior descending coronary artery that was subsequently treated with coronary stenting, whereas systolic compression of the artery occurred at the distal segment because of the existence of a systolic expansion of the left ventricular cavity at this level.3 The systolic compression of the left anterior descending coronary artery lumen caused by a systolic expansion of a left ventricular aneurysm has been previously reported.4
References
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