|Year : 2015 | Volume
| Issue : 4 | Page : 144-150
Schwarz type C myocardial bridge unraveled post-thrombus aspiration in a patient with hypertrophic cardiomyopathy
Satyajit Singh1, Aditya Kapoor2
1 Department of Cardiology, CARE Hospital, Bhubaneswar, Bhubaneswar, Odisha, India
2 Department of Cardiology, Sanjay Gandhi Post-Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
|Date of Web Publication||18-Dec-2015|
Department of Cardiology, CARE Hospital, Bhubaneswar, Plot No. 329/1929, Near Municipal Kalyan Mandap, Chandrasekharpur, Bhubaneswar, Odisha
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Hypertrophic cardiomyopathy (HCM), a heterogenous disease with diverse pathology and variable clinical course has a high prevalence of myocardial bridging. Despite the high prevalence of myocardial bridging in HCM patients, acute ST-elevation myocardial infarction (STEMI) due to concomitant atherothrombosis proximal to Schwarz type C myocardial bridge unraveled during trans-radial primary percutaneous intervention has rarely been reported in medical literature. Herein, we report a case of Schwarz type C myocardial bridge unmasked postthrombosuction in a patient with HCM presenting with acute STEMI. He had atherothrombosis proximal to the tunneled left anterior descending artery which was successfully stented with drug-eluting stent without the aid of intravascular ultrasound.
Keywords: Hypertrophic cardiomyopathy, primary percutaneous intervention, Schwarz type C myocardial bridge
|How to cite this article:|
Singh S, Kapoor A. Schwarz type C myocardial bridge unraveled post-thrombus aspiration in a patient with hypertrophic cardiomyopathy. Heart Views 2015;16:144-50
|How to cite this URL:|
Singh S, Kapoor A. Schwarz type C myocardial bridge unraveled post-thrombus aspiration in a patient with hypertrophic cardiomyopathy. Heart Views [serial online] 2015 [cited 2019 Feb 17];16:144-50. Available from: http://www.heartviews.org/text.asp?2015/16/4/144/172202
| Introduction|| |
Hypertrophic cardiomyopathy (HCM) is a common cardiac disorder, with an overall prevalence of 1:500 in the general population. A highly heterogenous disease with a diverse pathology and clinical course, HCM is the most common cause of sudden cardiac death in young people, including trained athletes. 
Adult patients with HCM may develop atherosclerotic coronary artery disease (CAD). Reports on the prevalence of CAD in HCM have varied, but up to 20% of adult HCM patients have been shown to have coexistent CAD.  Myocardial bridging of coronary arteries is a frequent congenital anomaly. The incidence of myocardial bridging in angiographic studies is 0.5-12%, and the prevalence of 30-80% in adults with HCM.  There have been reports insinuating that myocardial bridging may be associated with myocardial ischemia or infarction.  Myocardial infarction in a patient with both myocardial bridging and HCM due to interplay of myocardial bridging, concomitant atherosclerosis, and superimposed coronary thrombosis is not commonly reported in the medical literature. Treatment of symptomatic patients with myocardial bridging consists of pharmacological therapy although percutaneous intervention (PCI), myotomy or coronary artery bypass grafting can be considered.  However, concerns regarding perforation during stent deployment, stent fracture, in-stent restenosis, and stent thrombosis have limited their use in this condition. , Herein, we report a patient with HCM presenting with ST-elevation myocardial infarction (STEMI) with total occlusion of the left anterior descending artery (LAD) with successful transradial primary PCI.
| Case Report|| |
A 58-year-old nondiabetic, normotensive, nonsmoker male with no family history of CAD presented with retrosternal chest discomfort radiating to the back for past 6 h. He had no history of dyslipidemia, effort angina or rest angina in the past. On admission, blood pressure was 140/80 mm Hg with a regular heart rate of 100 beats/min. A grade III/VI ejection systolic murmur was noted in the aortic area. An electrocardiogram revealed sinus rhythm, normal axis and ST elevation in V1 and V2 leads [Figure 1]. Cardiac troponin-T level was 20.8 μg/L (normal reference value <0.1 μg/L). Echocardiogram revealed asymmetric septal hypertrophy, systolic anterior motion of anterior mitral leaflet, mild mitral regurgitation (MR), left ventricular outflow tract (LVOT) gradient of 55 mmHg; regional wall motion abnormality in LAD territory with thickness preserved and left ventricular ejection fraction of 66% [Figure 2], [Figure 3], [Figure 4] and [Figure 5]. A loading dose of aspirin 325 mg, clopidogrel 600 mg and atorvastatin 80 mg was administered, and patient was taken up for transradial primary PCI.
|Figure 1: Twelve lead electrocardiography of patient showing acute anterior wall myocardial infarction|
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|Figure 2: Parasternal long axis view M-mode: Asymmetric septal hypertrophy|
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|Figure 3: Parasternal long axis view M-mode: Systolic anterior motion of anterior mitral leaflet|
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|Figure 4: Apical 5 chamber view with continuous wave Doppler: Increased left ventricular outflow tract gradient|
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Coronary angiogram revealed total thrombotic occlusion of mid-LAD with no evidence of atherosclerosis in right coronary artery and left circumflex vessel [Figure 6] and [Figure 7]. The LAD was cannulated using a 6F extra backup support XB 3.0 guiding catheter (Cordis R Inc., USA) and the lesion in mid-LAD was crossed with J tipped. 014 inch Galeo floppy coronary guidewire (Biotronik Inc., Germany). Thrombosuction was done with 6F PRONTO V 3 extraction catheter (Vascular Solutions Inc., USA) [Figure 8]. Postthrombosuction, a residual stenosis of 70-80% was evident distal to first septal perforator and first diagonal with Schwarz type C myocardial bridge beyond second septal perforator and diagonal [Figure 9] and [Figure 10]. Resolute Integrity 3 mm × 23 mm (Zotarolimus eluting stent, Medtronic Inc., USA) was successfully deployed at 12 atmosphere for 30 s followed by poststent dilation with noncompliant balloon at 20 atmosphere for 20s. Utmost care was taken during stent placement so that distal edge of stent did not encroach into myocardial bridge [Figure 11].
|Figure 6: Left caudal angiographic view - total occlusion of left anterior descending artery|
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|Figure 7: Left anterior oblique cranial angiographic view - normal right coronary artery|
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|Figure 9: Myocardial bridge distal to second diagonal - systolic angiographic frame|
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There was no evidence of slow flow, no re-flow, immediate stent thrombosis or stent fracture post-PCI. The myocardial bridge became more prominent after stent deployment due to immediate improvement in myocardial contractility [Figure 12] and [Figure 13], however, there was no compromise in the flow. A follow-up echocardiogram 15 days later showed decrease in the LVOT gradient to 27 mm Hg and disappearance of MR. There were no symptoms of chest discomfort or dyspnea during follow-up.
| Discussion|| |
Myocardial bridging is defined as a segment of major epicardial coronary artery, the tunneled artery, that goes intra-murally beneath the muscle ridge. Myocardial bridge is seen in as many as 40-80% of cases of autopsy with functional myocardial bridging less commonly observed on coronary angiography (0.5-16%) ranging from 4 to 80 mm in length. Myocardial bridging occurs frequently in HCM, with reported prevalence as high as 30%.  Obstructive atherosclerotic CAD, involving one or more epicardial coronary arteries, has been reported to occur in 13% of HCM patients. 
Angina, myocardial ischemia, myocardial infarction, left ventricular dysfunction, myocardial stunning, paroxysmal atrioventricular blockade as well as exercise-induced ventricular tachycardia and sudden cardiac death are reported sequelae of myocardial bridging.  However, despite the high prevalence of myocardial bridging in HCM, these complications are rare.
Autopsy and intravascular ultrasound (IVUS) studies have revealed that the bridged and distal segments of bridged artery remain free from atherosclerosis while the proximal segment of the vessel is prone to developing atherosclerosis. Coronary segments immediately proximal to myocardial bridges have low wall shear stress, increased expression of vascular cell adhesion molecule 1, and dysfunctional, flat, polygonal endothelial cells predisposing to a pro-atherogenic milieu. ,, Separation of the bridged segment from perivascular adipose tissue in the epicardium that is associated with pro-inflammatory cytokines and adipokines offer a protective mechanism against atherosclerosis development in the tunneled segment. These factors likely contribute to plaque formation proximal to myocardial bridge and exert an atheroprotective mechanism inside the bridged segment.  This theory explains why our patient developed atherothrombosis proximal to the myocardial bridge while myocardial bridge and distal segment remained free of atherosclerosis.
In the presence of a proximal stenosis, myocardial bridge may only be identifiable after percutaneous transluminal coronary angioplasty when higher intravascular pressures and reversed hypokinesis of myocardium unmask myocardial bridging.  In our patient, Schwarz type C myocardial bridge became evident postthrombosuction with establishment of thrombolysis in myocardial infarction-III flow.
In the setting of primary PCI, concomitant HCM, Schwarz type C myocardial bridging and atherosclerotic stenosis, stent deployment is challenging because of perforation, stent fracture, in-stent restenosis, and stent thrombosis. Tsujita et al. evaluated PCI with predominantly drug-eluting stent (DES) in 70 patients with both myocardial bridges and LAD lesions and randomized them into 2 cohorts depending on whether the implanted stent ended proximal to a myocardial bridge or extended into the bridged segment. The target vessel revascularization was significantly higher in patients with stents extending into the bridge compared with patients with stents ending proximal to the myocardial bridge (29% vs. 3%). 
Therefore, any rationale for primary PCI in patients with concomitant atherosclerosis proximal to myocardial bridge in HCM would be to treat plaque with careful selection of stent size and accurate stent deployment, taking utmost care that distal edge of stent does not land in the bridged segment to prevent coronary perforation and stent fracture.
Careful selection of stent size by IVUS is recommended prior to performing coronary intervention in such patients. In our catheterization laboratory due to nonavailability of IVUS, we used our clinical judgement. We used several angiographic views and frames along with quantitative coronary angiography for accurate stent deployment proximal to the myocardial bridge in a patient with HCM with atherothrombosis. Myocardial bridge was unmasked postthrombosuction during transradial primary PCI.
| Conclusion|| |
Myocardial bridging occurs frequently in patients with HCM with generally benign prognosis. Acute STEMI due to the interplay of proximal atherothrombosis and Schwarz type C myocardial bridge in HCM patient undergoing primary PCI is rarely reported in the medical literature. There are myriad of strategies in elective management of symptomatic myocardial bridging in HCM patients, including DES implantation in the stenotic segment proximal to myocardial bridge using IVUS.
However, transradial primary PCI in HCM patients with 100% occluded coronary artery with a myocardial bridge unmasked only after thrombosuction is technically challenging with respect to stent sizing and accurate stent deployment. In our case, we successfully deployed DES without IVUS guidance in stenotic segment proximal to myocardial bridge unraveled only postthrombus aspiration.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13]