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Carotid intimal-medial thickness and endothelial
function in young patients with myocardial infarction.
Coppola G, Corrado E, Piraino D, Carella M, Muratori I, Camarda P, Di
Vincenzo A, Ciaramitaro G.F., Farinella M, Rotolo A, Evola S,
Hoffmann E, Assennato P, Novo S.
Chair of Cardiovascular Diseases, post-graduate School of Cardiology & Master of
Vascular Diseases, Division of Cardiology, Department of Internal Medicine and
Cardiovascular Disease, University Hospital, University of Palermo, Italy
INTRODUCTION
Myocardial infarction (MI) in adult patients under 45 years
old is a relatively unusual phenomenon (10% of AMI in the
U.S.A).
Most of these patients are men. Atherosclerotic coronary
artery disease is responsible for approximately 80% of cases.
Young patients with MI have a greater prevalence of
anatomically normal epicardial coronary arteries than older
ones. However, approximately 50% have single-vessel
atherosclerotic disease. The others have multivessel disease.
The prevalence of left main coronary artery stenosis is
approximately 5%. Multivessel disease is more likely in
patients with multiple risk factors and diabetes.
RISK FACTORS IN JMI
The most important modifiable risk factor is cigarette smoking.
Lipid abnormalities and a positive family history are also
important.
In young patients with MI who have not conventional
atherosclerosis risk factors, a search for other contributing factors
is warranted. The PAI-1 and plasma homocysteine levels should be
obtained.
Patient’s history should be reviewed for use of oral contraceptives
and cocaine.
The possibility of vasculitis or hypercoagulable states should be
considered. Embolization from the cardiac chambers, from
endocarditis, and from venous sources through a patent foramen
ovale are possible. Coronary dissection or congenital coronary
METHODS:
We enrolled 45 young adult patients (38 men and 7
female) with myocardial infarction (JMI), age 29-45,
mean age: 42±3years, and 45 healthy control subjects well
matched for sex and age.
• Standard questionnaire was used to obtain lifestyle and
clinical’s informations.
• A blood sample was drawn while the subject was fasting for
the measurement of glycaemia, cholesterol total, high-density
lipoprotein (HDL), and low-density lipoprotein (LDL)
cholesterol, triglycerides.
• All the subjects underwent high-resolution B-mode
ultrasound examinations for the measurement of the brachial
artery vasodilatory response after arterial occlusion (i.e.,
reactive hyperemia) and the intima–media thickness of
carotid arteries.
ULTRASOUND
EXAMINATIONS
According to the most recent
guidelines of the joint ESH we
considered normal patients
those with IMT < 0.9 mm,
patients with IMT those with
IMT between 0.9 mm and 1.5
mm and patients with
asymptomatic carotid plaque
(ACP) those with IMT > 1.5
mm.
Study Protocol
Endothelial function was evaluated according to the recent guidelines by
ultrasound using a 7.5-MHz linear-array transducer*.
Patients did not ingest substances that might affect flow mediated dilatation
(FMD) such as caffeine, or use tobacco for at least 6 h before the study. All
vasoactive medications were withdrawn for at least four half-lives, if possible.
Patients remained in the supine position for at least 10 min before the study
and were kept in this position during the procedure. The subjects have been
studied in a quiet, temperature-controlled room, in supine position.
The artery was scanned over a longitudinal section 3 to 5 cm above the elbow,
the site where the clearest image can be obtained. The focus zone was set to the
depth of the anterior vessel wall. Depth and gain settings were optimized to
identify the lumen-vessel wall interface.
The diameter of the brachial artery was measured from the anterior to the
posterior interface.
*Coretti MC et al., J Am Coll Cardiol 2002;39:257–65
Study Protocol
We evaluated the variation of the diameter of the brachial artery
at baseline, using high-resolution ultrasound, and after arterial
occlusion for 5 min through cuff inflation to at least 50 mmHg
above the systolic pressure.
The flow-mediated vasodilator response to reactive hyperaemia
was continuously recorded from 30s before to 5 min after cuff
deflation. Reactive hyperaemia (change in flow velocity) was
measured when compression was released, and the new arterial
diameter and flow velocity were measured one minute later.
Study Protocol
The percent change between the diameter at release of
compression (D2) and the baseline diameter (D1) is the so-
called flow mediated vasodilation (FMD).
Thus: FMD = (D2-D1)/D1 * 100. Ten minutes later, when
the artery returned to baseline, 300 mg of nitroglycerine
was administered and four minutes later arterial dilatation
was again measured.
The percent change between the postnitroglycerine
diameter (D3) and the baseline value (D1) is the so called
endothelium-independent vasodilation or nitroglycerine-
mediated vasodilation (NitroMV). Thus: NitroMV = (D3-
D1)/D1* 100.
Patients’ clinical and biochemical
characteristics
Variables %(N)
Sex (%M) 84% (38)
Cigarette smoking 56% (28)
N° of cigarettes 16±9
Hypertension 72% (36)
Waist circumference 101±11
Diabetes 28%(14)
Familiar History CVD 32% (16)
Glycemia mg/dl 126±58
Tot. Col. mg/dl 193±61
HDL-C mg/dl 42±9
LDL-C mg/dl 108±38
Triglycerides mg/dl 159±87
Fibrinogen mg/dl 416±84
Coronary arteriography results: number of
affected vessels
11%
7%
44%
38%
0 vessels 1 vessel 2 vessels 3 vessels
PREVALENCE OF CAROTID DISEASE
We observed a normal IMT only in 30% of patients with JMI in comparison
with 66% of control group, while 34% of patients showed an IMT in
comparison with 24% of controls, while carotid plaques were observed in 36%
of cases compared with 10% of healthy subjects.
70%
60%
50%
40%
30%
20%
10%
0%
Normal IMT Plaque
Controls Patients with JMI
CAROTID INTIMA MEDIA THICKNESS IN
PATIENTS WITH JMI IN COMPARISON TO
CONTROLS
p < .0001
2
Carotid IMT (mm)
1,5
1 1,47±0,78
0,5 0,95±0,41
0
patients with JMI Controls
We found an association between the two vascular beds (coronary and
carotid) with a corrispondence of 84% for patients in examination: in
particular in the 66% of the patients we found ATS in both areas and
in 18% of the cases in none of the two areas.
84%
70%
60%
50%
40% Both areas
None
30%
20%
10%
0%
Brachial artery diameter (BAD) and the flow
mediated dilatation FMD % in response to reactive
hyperaemia in patients with JMI and controls
Patients with JMI Controls P<
BAD (mm) 4,3±0,7 4,1±0,4 ns
FMD % 14±9 17±3 0,05
CORRELATION BETWEEN BRACHIAL-ARTERY
REACTIVITY AND CAROTID IMT IN SUBJECTS
WITH A JMI AND CONTROLS.
A significant inverse correlation was found between brachial-artery reactivity
and IMT of the common carotid artery in the subjects with JMI (r=–0.663,
P=0.0001) but not in the control subjects (r=–0.223, P=0.161).
JMI Controls
25
25
P = .00001 P = .161
20
20
15
15
10
10
5
5
0 0
0,5 1,0 1,5 2,0 2,5 3,0 0,5 1 1,5 2
Carotid IMT Carotid IMT
Association Between Coronary
Atherosclerosis Disease Severity And FMD %
0 vessels 1 vessels 2-3 vessels
20
16
FMD %
12
8
4
0
Association between CAD Severity
and Extra-coronary Disease
5,0
4,0 P <.001
Carotid IMT mm
3,0
2,0
1,0
0,0
1 vessel 2 vessels 3 vessels
Regression Analysis :Baseline parameters in
relation to severity of CAD
Variable r P value
BMI .275 0,05
Carotid IMT (mm) .349 0,01
N° of daily smoked cigarettes .486 0,0001
CONCLUSIONS
Atherosclerosis is known to be a systemic process that
involves different arterial districts.
The current study demonstrates an association between
structural changes and functional changes related to early
atherosclerosis in a group of subjects with JMI.
The examination of arterial-wall structure/function in
young persons with the use of noninvasive
ultrasonographic methods may provide important
information on early changes in the course of developing
atherosclerosis, especially in persons at high risk for
cardiovascular disease.
Carotid intimal-medial thickness and endothelial
function in young patients with myocardial infarction.
Coppola G, Corrado E, Piraino D, Carella M, Muratori I, Camarda P, Di
Vincenzo A, Ciaramitaro G.F., Farinella M, Rotolo A, Evola S,
Hoffmann E, Assennato P, Novo S.
Chair of Cardiovascular Diseases, post-graduate School of Cardiology & Master of
Vascular Diseases, Division of Cardiology, Department of Internal Medicine and
Cardiovascular Disease, University Hospital, University of Palermo, Italy
Int Angiol. 2009 Apr;28(2):120-6.
Contact: Dr. Giuseppe Coppola MD, PhD (g.coppola@unipa.it)
