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Insignificant May Be Significant ‼
BUT
How To Know ??
Dr. ELSayed Farag (MD)
Quated from ACC (Cath of the month)
Chief Complaint: A 69-year-old male
presented to hospital with complaints of
chest pain and shortness of breath. On
initial exam, he was noted to be severely
hypertensive with a blood pressure of
200/111 mm Hg and in pulmonary edema
Past Medical History:
He has a history of hypertension and
hyperlipidemia
Let us see his initial
ECG
What does it show ??
A. Lateral ST elevation
B. Anterior ST elevation
C. Inferoposterior ST elevation
D. Pericarditis
B. Anterior ST elevation
What is the best plan of initial treatment ?
A. I.V nitroglycerine , Frusemide ,Aspirin then
I.V thrombolysis.
B. I.V nitroglycerine , Frusemide ,Aspirin
,clopidogrel then I.V thrombolysis.
C. I.V nitroglycerine , Frusemide ,Aspirin
,clopidogrel,heparin ,abciximab then 1ry PCI
D. I.V nitroglycerine , Frusemide ,Aspirin
,clopidogrel,heparin ,abciximab plus I.V
thrombolysis
What did his coronary angio.show ?
A. A…Proximally occluded LAD with mild
irregularities in the LCX and RCA.
B. Mid occluded LAD with mild irregularities in the
LCX and RCA.
C. Proximally occluded LAD with mild irregularities
in the LCX and signficant mid RCA lesion.
D. Proximally occluded LAD with normal LCX and
RCA.
A. Proximally occluded LAD with mild
irregularities in the LCX and RCA.
What is the best size of the stent ?
A. 3.5 mm X 10 mm
B. 3 mm X 20 mm
C. 3 mm X 15 mm
D. 3.5 X 15 mm
C. 3 mm X 15 mm
The patient did well post-intervention.
Transthoracic echo showed the left
ventricular ejection fraction to be 30% with
a thinned and akinetic mid-to-apical
septum, true apex, and apical lateral wall.
No discrete aneurysm or thrombus was
noted. The mid posterior wall was
hypokinetic as well.
What is best suitable discharge
medications ?
A. Oral anticogulation, aspirin , clopidogrel , small
dose BB , ACEI , statins ,frusemide and nitrate .
B. Aspirin , clopidogrel , small dose BB , ACEI ,
statins ,frusemide and nitrate .
C. Oral anticogulation, aspirin , small dose BB ,
ACEI , statins ,frusemide and nitrate .
D. Aspirin , clopidogrel , ACEI , statins ,frusemide
and nitrate .
The patient did well after discharge and on a
follow-up visit, one month later, with his
primary care physician, was noted to be
without chest pain, shortness of breath,
dyspnea on exertion, paroxysmal nocturnal
dyspnea, or orthopnea. He was tolerating his
medications, his international normalized ratio
was therapeutic (2.2) and he was not having
any problems with bleeding or excessive
bruising.
Unfortuntely, the following morning the
patient awoke acutely short of breath and with
chest pain. He again presented to the hospital.
Initial exam showed the patient to be in
pulmonary edema.
Initial ECG showed anteroseptal ST elevations
which were unchanged from an ECG done
prior to discharge.
BUT
What about the subsequent ECG ?
What does it show ?
A. The previous anterior MI only
B. The previous anterior MI plus inferior
ST elevation
C. Inferior and lateral ST elevations
D. Inferoposterior ST elevation
B. The previous anterior MI plus
inferior ST elevation
What is the best dicision ?
A. Stabilize the pt.medically then follow
up
B. Take the patient directly to the
cath.lab.
C. Stabilize the pt.medically then cardiac
catherization
D. The patient should take the I.V
thrombolysis in the ambulance.
C. Stabilize the pt.medically then
cardiac catherization
What is the expected problem ?
A. Stent occlusion by thombus
B. RCA occlusion by thrombus with
patent stent
C. LCX occlusion with in stent stenosis
D. LCX and RCA occlusion with patent
stent
B. RCA occlusion by thrombus with
patent stent
The patient’s left ventricular end-
diastolic pressure was 42 mm Hg. An
intra-aortic balloon pump and TPM
were placed and the RCA was then
successfully stented .The patient did
well post-intervention.
What are the important thrombophillia
workup to be done in that patient ?
A. Protein C and S levels.
B. Factor V Leiden mutation , PAI-
1 levels , Lp(a) & homocysteine.
C. Aspirin resistance.
D. All of the above
D. All of the above
Workup while in the hospital demonstrated
normal protein C and S levels, no evidence of
the factor V Leiden mutation normal PAI-1
levels, and the absence of aspirin resistance .
His total cholesterol was 133, total glucose 96,
HDL 31, and LDL 83. However, the patient’s
lipoprotein(a) level was markedly elevated at
>95 (normal <30) and his homocysteine level
was 18.4 (normal 6.1-16.3).
Rupture of nonocclusive plaque
A. Accounts for nearly 50 % of fatal coronary
events.
B. Accounts for nearly 25 % of fatal coronary
events.
C. Accounts for nearly 95 % of fatal coronary
events.
D. Accounts for nearly 75 % of fatal coronary
events.
D. Accounts for nearly 75 % of fatal
coronary events.
TAKE HOME MESSAGE
This case illustrates two very important
concepts. First, progressive luminal narrowing
is not the cause of the majority of acute
infarcts. Identifying which nonobstructive
coronary stenoses are likely to rupture
suddenly is an active area of research.
Second, patients with lipoprotein(a) levels >30 mg/dl
have a threefold greater prevalence of coronary heart
disease and more frequent restenosis following
angioplasty and increased vein graft stenosis. Despite
this increased risk, the clinical efficacy of reducing
lipoprotein(a) levels in patients with established
coronary artery disease remains uncertain. Levels are
best lowered with nicotinic acid and estrogens.
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