Transcript myocardial bridge

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 nonspecific ST-T changes. Elevated cardiac
enzyme was found (CPK: 992 IU/L; CKMB: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)
1200
1000
800
600
400
200
0
992
705
CK
CK-MB
523
37
1st
13
2nd
24
3th
100
9
4th
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
WBC: 10800
Hgb: 12.5
Platelet: 65000
TP: 6.0
Albumin: 2.8
GOT: 604
GPT: 271
TCH: 344
TG: 991
91-8-30
=> 3710
=> 14.7
=> 92000
=> 8.8 g/dl
=>3.7 g/dl
=> 44 IU/L
=> 45 IU/L
=> 122 mg/dl
=> 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 emboli..)
Coronary arteritis ( Kawasaki dx, RA, AS…)
• Dissection into coronary artery ( aortic dissection )
• Congenital anomalities of coronary circulation
( myocardial bridge, coronary AV fistula)
• Coronary trauma (myocardial
contussion ,iatrogenic…)
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
cardiomyopathy
• Myocardial bridging can exist in any coronary artery,
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 102:283,1982
Kramer et al
• (Degree of angiographic systolic compression of
the bridge)
•
• EKG
Gr I (0~30%) Gr II(31~50%) Gr III(51~100%)
-
25 %
30 %
33%
• => As the systolic compression worsened,
the objective evidence of ischemia
increased
• Thallium
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