Myocardial Infarction Associated with Myocardial bridging and

Hypertrophic Cardiomyopathy

大林慈濟心臟內科林志達醫師

Basic Information

• Name: 章 X勝• Age: 48 y/o

• Sex: Male

• Chart number: P102312131

• Date of admission: 91-05-24

• Date of discharge: 91-05-31

Admission History (I)

• The 48 y/o male patient was diagnosed to have DM and HTN for years without regular treatment.He suffered from exercise-related chest tightness for 1 year. It could be relieved by rest. He experienced of severe chest tightness with cold sweating in the morning of admission. He was brought to our ER, where low blood pressure (88/48 mmHg) and tachycardia (116 bpm) were noted.

Admission History (II)

• EKG showed sinus tachycardia and non-specific ST-T changes. Elevated cardiac enzyme was found (CPK: 992 IU/L; CK-MB:37 IU/L). Non-ST elevation MI with was diagnosed based on the clinical symptoms and cardiac enzyme data. Patient was sent to cath room for further evaluation and treatment.

Past History

• DM for 1 year with irregular treatment

• HTN for 4 years with irregular treatment

• Chronic hepatitis C (+)

• No major operation history

• Smoking(-), alcohol consumption(+)

• No allergy history

Risk factors for CAD

• DM

• HTN

• Hyperlipidemia

• Male

Physical Examination(I)

• BP: 88/48 mmHg, HR: 116 bpm, BT: 36.6 C, RR: 18/min

• Consciousness: E4V5M6

• Conj: not pale; Sclera: icteric

• Neck: JVE(-), LAP(-)

• Chest: symmetric expansion, BS: clear

Physical Examination(II)

• Heart: PMI: LMCL, 4th LICS, RHB, Gr III systolic murmur at L2~3 ICS, S3(-), S4(-)

• Abdomen: soft, no tenderness, BS: normoactive, liver/spleen: impalpable

• Ext: freely movable, warm,no edema

Laboratory finding

• WBC: 10800, RBC: 3.61, Hgb: 12.5, MCV: 90, PL:65000

• GOT: 604, GPT: 271, GGT: 1049, ALP:221, DBI:4.5, TBI: 6.3 AFP: 5.09, Anti-HCV:(+) HBsAg: (-)

• BUN: 7, Cr:2.0, TP:6.0, ALB:2.8, TCH: 344, TG: 991, UA: 8.0, Na: 127, K: 2.73, Glu:416, Osmo:295

Other Examination

• CXR: To be presented

• EKG: To be presented

• Cath: To be presented

• Abdominal echo: mild fatty liver.

Tentative Diagnosis(I)

• Acute myocardial infarction with shock • Hypertension• Diabetes Mellitus• Alcoholic liver disease with thrombocytopenia

and jaundice, anti-HCV(+)• Renal insufficiency• Hyperlipidemia, Hypoalbuminemia• Hyponatremia, Hypokalemia

Treatment Course (I)

• Because AMI with cardiogenic shock was diagnosed at ER, patient was sent to cath room immediately. Coronary angiogram revealed patent coronary arteries but severe myocardial bridging at middle LAD. Cardiac echo showed obstructive type hypertrophic cardiomyopathy with good LV performance. Dopamine was used to maintain blood pressure initially and was tappered soon.

Treatment Course (II)

• After blood pressure became stable, verapamil was added to control heart rate and decreased heart contractility. After heart rate was controlled, heart murmur disappeared and follow-up cardiac echo revealed disappearance of LVOT pressure gradient & SAM. No more chest tightness was complained and patient was discharged.

• Currently the patient was receiving follow-up at OPD.

Cardiac enzyme(Normal range CK: 56~244; CK-MB: 7.9~17.3)

992

705523

10037 13 24 90

20040060080010001200

1st 2nd 3th 4th

CK

CK-MB

Cardiac Echo

• Normal chamber size• No regional wall motion abnormalities• Good LV performance, Mitral flow E<A• Increase LVOT velocity ( pressure gradient: 35

mmHg), ASH(+) (IVS: 19 mm, LVPW: 12 mm), SAM(+)

• C/W Obstructive type hypertrophic cardiomyopathy with mild~modertae MR

Tc-99m Myocardial Infarction Study

• Tc-99m myocardial infarction study: normal myocardial scan. There is no evidence of acute myocardial infarction , ventricular aneurysm or myocardial contusion

Lab Data Follow-up

• 91-5-24 91-8-30• WBC: 10800 => 3710• Hgb: 12.5 => 14.7• Platelet: 65000 => 92000• TP: 6.0 => 8.8 g/dl• Albumin: 2.8 =>3.7 g/dl• GOT: 604 => 44 IU/L• GPT: 271 => 45 IU/L• TCH: 344 => 122 mg/dl• TG: 991 => 40 mg/dl

Current Drugs

• Verapamil (40mg) 1# TID

• Concor 1# QD

• Glipizide 1# QDAC

• Atorvastin 1# QD

• Silymarin 1# BID

• Sennoside 2# HS

Discussion

• 1. Cause of AMI

• 2. Review of myocardial bridging

• ---Introduction

• --- Clinical presentations

• --- Treatment

Causes of Myocardial Infarction(I)

• Coronary atherosclerosis---the most common• Coronary artery spasm• Coronary embolism ( IE, prosthetic valve embol

i..) Coronary arteritis ( Kawasaki dx, RA, AS…)• Dissection into coronary artery ( aortic dissection )• Congenital anomalities of coronary circulation ( m

yocardial bridge, coronary AV fistula)• Coronary trauma (myocardial contussion ,iatrogen

ic…)

Causes of Myocardial Infarction(II)

• Coronary mural thickening with metabolic disease ( amyloidosis, coronary fibrosis by R/T…)

• Myocardial oxygen demand-supply disproportion ( Aortic stenosis, CO poisoning, thyrotoxicosis, prolonged hypotension)

• Hematological dx ( polythemia vera, thrombocytosis, DIC, TTP…)

• Miscellaneous (cocaine abuse…)

Myocardial bridging

Introduction (I)

• The coronary arteries may dip into the myocardium for varying lengths and then reappear on the heart’s surface. The muscle overlying the intramyocardial segment of the epicardial coronary artery is termed a myocardial bridge, and the artery coursing whthin the myocardium is called a tunneled artery.

Introduction (II)

• Myocardial bridging was first recognized 200 years ago by Reyman (1737), again reported in 1922.

• Myocardial bridging is a frequent congenital anomaly with an incidence 5~86% at autopsy study.

• 0.5~12 percent in angiography study• 30~80 percent in adults with hypertrophic cardiomy

opathy• Myocardial bridging can exist in any coronary arter

y, but the LAD is the most commonly involved.

Introduction (III)

• The bridging segment can vary in length from less than 1 cm to long segments involving the majority of the length of the vessel. Usually, there is only one segment in a single artery involved, but there have been reports of multiple segments of arteries bridged, or multiple arteries affected in a single individual.

Bridging vs Atherosclerosis

• Polacek published data in 1961 that the site of bridging is protected from atherosclerosis, but the segments immediately proximal to the bridges had a significantly greater degree of atherosclerosis compaired to the remainder of the vessel.

Clinical Presentation(I)

• Asymptomatic, myocardia ischemia (angina, myocardial infarction, arrhythmia, sudden death)

• Clinical presentations were descided based on three factors:

• (1) length of the tunneled coronary segment• (2) degree of systolic compression• (3) heart rate

Clinical Presentation(II)

• Longer tunneled segments of coronary arteries, more severe systolic diameter narrowing of the tunneled segment, and tachycardia may controbute to the introduction of myocardial ischemia.

Am Heart J 102:283,1982Kramer et al

• (Degree of angiographic systolic compression of the bridge)

• Gr I (0~30%) Gr II(31~50%) Gr III(51~100%)

• EKG - 25 % 30 %

• Thallium - - 33%

• => As the systolic compression worsened, the objective evidence of ischemia increased

Treatment

• Asyptomatic => No treatment

• Myocardial ischemia

• (1) Medical treatment: beta blockers or calcium channel blockers( control tachycardia and antispasmodic effects)

• (2) Stenting

• (3) Surgery: supraarterial myotomy

Treatment (II)

• Nitrates have been shown to exacerbate the systolic obstruction and worsen symptoms. There may be a compensatory increase in heart rate and contractile force due to the lowering of SBP by the nitrates, or vasodilatation may occur in the non-bridged segments, but not in the myocardial bridge exacerbating the compression stenosis.

References

• 1. Myocardial bridging and hypertrophic cardiomyopathy: relief of ischemia by surgery ( International Journal of Cardiology, 8 :327~330; 1985

• 2. Myocardial infarction associated with myocardial bridging (Cathet Cardiovasc Dioag 40: 364~367;1997