NSTE-ACS

ACS represent life-threatening manifestation of atherosclerosis .

It is usually precipitated by acute thrombosis induced by ruptured or eroded atherosclerotic coronary plaque , with or without concomitant vasoconstriction causing sudden and critical reduction in blood flow . In the complex process of plaque disruption ,inflammation was revealed as key pathophysiologic element .in rare cases, ACS may have atherosclerotic etiology such as arteritis ,trauma, dissection ,thrombo-embolism ,congenital abnormality , cocaine abuse or complication of cardiac catheretization.

PATIENT PRESENTATION

Chief Complaint:

“my chest discomfort is gone now that they put a stent in my coronary artery”.

History of Present Illness: JW is a 66-year-old male who presented to the emergency department by ambulance at 14:00 complaining of 4 hours of continuous chest pressure that started while raking leaves. JW developed substernal chest pressure at 10:00 about 30 minutes after starting to rake leaves at his home. He stopped and rested but the chest pressure did not resolve. Local paramedics were summoned, and he was given three 0.4 mg SL NTG tablets by mouth, 325 mg Aspirin by mouth, and morphine 2 mg IV push at 13:30 without relief of chest discomfort. He was brought to the ED by ambulance. A 12-lead ECG was performed, and NTG 10 mcg/min IV infusion was initiated at 14:15. the cardiology attending consulted with the interventional cardiologist and the decision was made bring JW to cardiac catheterization laboratory for coronary angiography.

Bivalirudin was initiated at the time of PCI and was discontinued in the cardiac catheterization lab following successful PCI. The patient is now in the CCU s/p PCI with placement of a bare metal stent in the LAD coronary artery.

Past Medical History:

HTN X 5 years.

Family History:

Father with MI at age 75; mother and sister alive with 2 DM.

Social History:

Retired former newspaper reporter.

Tobacco/Alcohol use:

Non smoker. Denies use of alcohol or illicit drug.

Allergies/intolerances/adverse drug events:

Non.

Medication (current):

NTG 10 mcg/min IV.

Medication taken prior to admission:

Amoldipine 10 mg PO once daily

ASA 325 mg PO daily.

Review of system:

Previous 10/10 chest pressure now 1/10; (-) nausea, abdominal pain, or headache.

Physical Examination General:

Elderly male in less distress.

Vital Signs:

BP 140/90 mm Hg, P 88 bmp, RR 17, T 37 C

Weight (90 kg)

Height (180 cm)

Denies pains, but 1/10 chest pressure.

HEENT:

Normal; (-) AV nicking, (-) papilledema

Chest :Clear to A&P, JVD 4 cm, PMI left midclavicular line 4th intercosal space.

Cardiovascular:

RRR, normal S1,S2, (-) S3 or S4, (-) M/R/G.

Abdomen:

Not tender /not distended , normal bowel sounds.

Neurologic :

A&O x3 , cranial nerves II-XII intact.

Genitourinary:

Deferred

Rectal:

(-) occult blood.

Extremities:

No bruits, pulses 2+ ,(-) edema

Laboratory Tests:Sodium ---------- 140 mEq/L. Plt ------------- 220 x 10^3/mm^3

Potassium ------ 4.2 mEq/L WBC---------- 4.3 x 10^3/mm^3

Chloride --------- 105 mEq/L Troponin1---- 7.5 ng/ml

CO2--------------- 24 mEq/L LDL-C---------110 mg/dl

BUN---------------16mg/dl TG-C----------- 240 mg/dl

SCr---------------- 1.0 mg/dl HDL-C--------- 35 mg/dl

Glucose---------- 99 mg/dl Mg-------------- 2.0 mEq/L

Hgb----------------14.7 g/dl AST------------30 U/L

Hct-----------------44.0% ALT-------------30 U/L

INR----------------1.0 O2 sat----------99%

ECG:

In the ED showed sinus tachycardia with 2mm ST depression in leads V2-V4; normal PR , QRS ,and QTc intervals; post PCI ECG shows NSR with resolution of ST depression , no Q wave.

Assessment:

66 year old male with signs , symptoms and laboratory tests consistent with ACS .

Targeted Questions :

1- what type of ACS is this?

Non ST segment elevation myocardial infarction.

2-whats the signs and symptoms of ACS dose this patient have?

this patient suffer from prolonged chest pain and pressure .

3- what are this patient risk factors for developing CHD?

HNT ,age > 60, and prior CAD (PCI) .

4- how is the diagnosis of MI made?

A –physical examination :the goal from this to exclude non cardiac causes of chest pain and non ischaemic cardic disorder.

B- 12- leads ECG (the first line diagnosis) : It should be obtained within 10 min after first medical contact. The characteristic ECG abnormalities of NSTE –ACS are :

ST –segment depression ,or transient elevation and or T-wave changes (inversion).

C- biomarker:

Elevation or reduction of troponin1or t within ~ 4 h after symptom onset (more sensitive and specific ).

6- if this patient had chronic kidney disease. How would this influence your choice of anticoagulant and dose?

Enoxaparin:

Dose reduction to 1 mg/kg once daily in the case of sever renal failure ( Crcl < 30 ml/min) consider monitoring of anti-Xa activity.

Fondaparinux:

Contraindicated in sever renal failure (CrCl < 20 ml/min)

Drug of choice in patient with moderately reduced renal function (CrCl 30-60 ml/min ).

Bivalirudin :

Patients with moderate renal impairment (30-59 ml/min) should receive an infusion of 1.75 mg/kg/h if the CrCl is <30 ml/min , reduction of the infusion rate to 1 mg/kg/h should be considered . No reduction in the bolus dose is needed . If patient is on haemodialysis , the infusion rate should be reduced to 0.25 mg/kg /h.

UFH infusion adjusted to aPTT is recommended when CrCl<30

Ml/min with most anticoagulant .

7- in which patient sub groups is the benefit in cardiovascular death, MI , or stroke not greater than the risk of major bleeding in patients treated with prasugrel vs clopidogrel following PCI ?

-there was evidence of net harm with prasugrel in patients with history of cerebrovascular events .in addition there was no apparent clinical benefit in patients > 75 years ago or low body weight <60 kg .

8- what is the minimal duration of time that dual antiplatelet therapy should be continued?

-Minimum time equal 6 month .

9- how is the dose of B-blocker titrated?- Target resting HR 50-60 bmp metoprolol : 5 mg increment by slow (1-2 min) IV , followed in 1

to 2 h (25-50 mg )by mouth every 6-8 h. Propanolol: 0.5-1 mg IV dose followed in 1 to 2 h by (40-80 mg

PO ) every 6-8 h. Atenolol: 5 mg IV dose followed 5 min later by second 5 mg IV

dose & then 50-100 mg PO every day .

10- how would your selection of pharmacotherapy differ if this pt presented with symptoms of acute heart failure?

B-blocker and ACEI (or ARB) appropriately titrated are indicated in pt with NSTE-ACS and LVD with or without symptoms of HF.

Aldosterone inhibitor ,preferably eplerenone are indicated in pt with NSTE-ACS , LVD & HF.

11- what is the single best predictor of mortality in this patient?

- Left ventricular dysfunction (or HF) by Echo or 12-leads ECG.

12- the Pt present to his cardiologist 2 weeks following discharge . His BP is 142/90 mm Hg , pulse 55 bmp , and he is afebrile . His chemistry panel include K+ of 4.2 mEq/L and SCr 1.07 mg/dl, what recommendation would you make to the physician regarding his pharmacotherapy?

-you must stop increament of B-blocker to prevent further reduction of HR.

13- the patients presents to his cardiologist 6 weeks following discharge . The pt LDL-C is 68 mg/dl , but his fasting TG are still elevated at 185 mg/dl and HDL-C still low at 36 mg/dl . What recommendation would you make to the physician regarding his pharmacotherapy regimen?

- Should be administered with Gemfibrozil to reduce TG and TO increase HDL-C.

References:

1- ESC guideline 2011 .

2-pharmacotherapy textbook by depiro .

3- Circulation Journal of AHA 2012 .