Intern Case Report Talitha Morton, PGY1 CC: Chest

Intern Case Report Talitha Morton, PGY1 CC: Chest

Intern Case Report Talitha Morton, PGY1 CC: Chest pain 61 yr old male presented to ED w/ substernal, non-radiating chest pressure while walking that lasted approximately 30 minutes. Bilateral arm numbness and weakness. Bilateral LE edema last night. Now resolved. Severe muscle aches x 1 month

Chest discomfort resolved after taking Imdur. Did not take NTG SL d/t concern for hypotension. Denied shortness of breath, nausea or PMHx: ASA 81 mg

Effient 10 mg CAD daily Recent MI Recent cardiac Atorvastatin 40 mg daily arrest d/t Diltiazem 120 sustained mg daily ventricular tachycardia s/p Imdur 30 mg AICD

daily implantation Protonix 40 mg HLD daily Allergies: Lisinopril Metoprolol Surgical Hx: AICD

Social Hx: Former tobacco user; recently quit smoking No alcohol or drug use Family Hx: None Vital signs: Labs:

T: 98.4 P: 68 BP: 124/64 RR: 18 O2: 98% RA CBC: H/H 12.6/36.4 CMP: unremarkable Troponin: 0.20 BNP: 61.8 CK: 59 TSH: 0.38

FT4: 1.11 ESR/CRP: 35/8.6 UDS: +BZD. Confirmation test (-) Imaging: CXR: mild bibasilar interstitial prominence may be acute or chronic Echo: LVEF 62%. Normal chamber size and wall thickness. Normal global systolic function.

EKG Physical Exam: Started on heparin gtt and given ASA 325 mg in ED Assessment/Plan: NSTEMI DAPT w/ ASA and Effient, heparin gtt, Imdur and diltiazem and NTG SL prn Start lisinopril . Hold beta-blocker. Trend troponin Echo and Cardiology consult

Obtain records from OSH Myalgias CK normal. Start Flexeril. Consider changing atorvastatin to pravastatin. Hx of cardiac arrest d/t VT s/p AICD HTN OSH medical records- EKG OSH medical

records Admitted 1 month prior to presentation to BSW with complaint of chest pain Acute anterior wall STEMI with troponin peak 1.99 Coronary angiography: Left main: no significant stenosis LAD: 100% proximal occlusion with TIMI 0 flow. DES x2 to LAD. LCx: no significant disease RCA: no significant disease

Echo: LVEF 45%. Hypokinesis if apical septum, apex and mild hypokinesis of anterior wall Cont. Repeat admission within one week after discharge with recurrent chest pain NSTEMI Coronary angiography: LM: 50% diffuse disease. Suspicious for residual dissection from previous stent placement. DES x1 to LM

LAD: patent stents LCx: 90% stenosis w/ TIMI 2 flow DES x1 to LCx Cont. On 2nd hospital day the patient experienced cardiac arrest due to VT/VF with brief resuscitation EP study and AICD implantation for inducible VT/VF Cont. Recurrent chest pain after AICD

placement: Coronary angiography: LM: patent stent LAD: patent stents. 70-75% stenosis distal to stent. Improved to 30% with IC NTG. Residual area of spasm noted. Diagonal: 85% stenosis w/ TIMI 1 flow. Improved to TIMI 3 flow with IC NTG. LCx: stent patent 1st OM: occluded w/ TIMI 0 flow. Improved to 30% stenosis and TIMI 3 flow with IC NTG.

Hospital Day 2 No chest pain or shortness of breath. +myalgias. Troponin 0.20 0.98 3.72 7.07 Cardiology recommendations: Increase Imdur 60 mg daily and diltiazem 180 mg daily for hx of coronary vasospasm Cont lisinopril to decrease endothelial inflammation Change to rosuvastatin 10 mg daily. Statin therapy will reduced inflammation and reduce incidence of vasospasm. Plan for coronary angiography

Coronary angiography: Triple-vessel CAD Patent stents of LM, proximal LAD and mid-LAD Significant coronary artery spasm in LCx. 70-80% stenosis improved to 30% after IC NTG. 20-30% stenosis of proximal and mid-RCA Plan: Optical coherence tomography (OTC) of area of LCx and mid-distal LAD w/ possible intervention given refractory vasospasms despite aggressive medical management resulting myocardial necrosis and malignant dysrhythmias

OCT and IVUS Evaluate for atherosclerotic coronary disease X-ray coronary angiography w/ contrast media OCT and IVUS: Utilizes light vs sound to create an image. Contour of vascular lumen and allows for visualization of the vascular wall. Coronary angiography may be limited in assessment of the extent of atherosclerotic disease due

to: Diffuse atherosclerosis: No focal encroachment of the lumen Complex luminal shapes: varying severity in multiple views Compensatory enlargement: Optical coherence tomography (OCT) Intravascular Three concentric layers ultrasound (IVUS) Elastic membrane Three-layer

(internal), media appearance (middle) and external Intima (bright), media elastic lamina (outer) (dark) and adventitia (bright) OCT report: LCx: patent vessel with atherosclerotic plaque noted in area of spasm correlated with angiography PCI w/ DES x1 to LCx

Mid-distal LAD: No significant atherosclerotic disease in area of spasm correlated with angiography Hospital Day 3 Chest pain x2 overnight that resolved spontaneously within minutes Troponin 6.39 8.35 13.27 SBP 80-90s Cardiology recommendations: Start Ranexa 500 mg BID. Later increased to 1000 mg BID. Monitor for worsening hypotension

Hospital Day 4-5 No chest pain overnight. Improved muscles aches. Troponin 9.14 7.68 6.54 Cardiology recommendations: Continue current regimen Remained asymptomatic overnight. Discharged on hospital day 5. ASA and Effient, Imdur, diltiazem, lisinopril, Ranexa, rosuvastatin and NTG SL prn

Follow-up Twelve days later: Admitted for lightheadedness, hypotension and AKI Reduced Imdur and lisinopril dosages Three additional admissions over four months for NSTEMI presumably d/t coronary vasospasm Repeat Echo: Mildly reduced LV systolic function with LVEF of 4550% and hypokinesis of antero-apex c/w injury/ischemia Variant angina

Prinzmetal or vasospastic angina First described by Prinzmetal et al. in 1959 Characteristics: Usually younger, females with w/o traditional risk factors for CAD, except tobacco use Episodes of angina pectoris, usually at rest and often between midnight and early morning. Usually lasting 5-15 minutes. ST-elevation on EKG Focal spasm of smooth muscle layer of arterial wall leading to high-grade obstruction causing

transient ischemia or myocardial infarction, in some cases. Pathogenesis Vascular smooth muscle hyperreactivity May be focal, more than one site or diffusely Normal vessel or at the site of atherosclerotic plaques Vasoconstrictors that provoke spasm: acetylcholine, serotonin, histamine, noradrenaline and dopamine

Autonomic nervous system Imbalance of vagal and sympathetic tone. Vagal tone often higher from midnight to early morning. Risk Factors Tobacco use* Ephedrine-based products Cocaine, marijuana, amphetamines, alcohol, butane and sumatriptan Guide-wire or balloon dilation

during PCI Magnesium deficiency Hx of vasospastic disease Migraines, Raynauds phenomenon and aspirin-induced asthma Diagnosis 12-lead EKG Acute episode: Transient ST elevation in multiple leads (<15 mins) TWIs, tall and broad R wave, absence of S wave, taller T wave, negative U wave

Serial cardiac enzymes Coronary angiography: Transient ST-elevation At least 50% obstruction at site of spasm that is reversed with IC NTG Provocation tests: Acetylcholine and hyperventilation (rarely used) Cont. No ST-elevation present Stress test exclude obstructive coronary disease Most will be normal. 10-30%

exercise-induced spasm during stress test. Ambulatory EKG Detect ST-elevation with or without angina Can also be used to assess efficacy of therapy because asymptomatic episodes are common Differential Dx Fixed obstructive CAD Hx consistent with variant angina GERD with esophageal spasm

Cardiac X syndrome Angina or angina-like chest pain with exertion and normal coronary arteries without evidence of vasospasm. EKG: ST depression with EST Proposed pathogenesis: Coronary microvascular dysfunction Sensitive heart syndrome. Enhanced sensitivity to intracardiac pain. Differential Dx ST-elevation Acute pericarditis

Stress-induced cardiomyopathy Non-cardiac chest pain w/ early repolarization Ventricular aneurysm post-MI LVH LBBB Brugada syndrome Management Goal is to reduce frequency of symptomatic episodes and serious complications NTG SL: reduce duration of episode and

ischemia Smoking cessation Nitrates and CCB will prevent vasoconstriction and promote coronary artery vasodilation Long-acting nitrates may lead to nitrate tolerance Indicated if continued symptoms on CCB or persistent asymptomatic episodes to reduce risk of ventricular arrhythmia CCBs: nefedipine, diltiazem (240-360 mg

Cont. Magnesium: Single study. Vasodilation with IV Mg and had reduced chest pain and ST-elevation with acetylcholine provocation PCI: Possible benefit in medically refractory vasospasm that is associated with mild to moderate obstructive CAD and when the vasospastic segment can be clearly identified

Recommend to avoid: Non-selective beta-blockers ASA at high doses d/t inhibition of prostacyclin production. ASA 81 mg in CAD Complications 25% untreated patients: MI and arrhythmias Acute myocardial infarction Usually with fixed-obstructive CAD Arrhythmias

Heart block RCA Due to AV-node ischemia Ventricular tachycardia LAD Recommend AICD placement in sudden cardiac arrest Cont. VT with high-risk features: Fixed-obstructive CAD Large ST-elevation Multi-vessel spasm on maximal or even submaximal

doses of CCB Refer for EP study/possible AICD VT without high-risk features: Maximize CCB dose and refer for EP study/possible AICD Maximize CCB dose and monitor closely for arrhythmias Prognosis Infarct-free survival at 10-years is >80% Worse prognosis associated with

obstructive CAD and multi-vessel spasms The End References Intravascular ultrasound, optical coherence tomography, and angioscopy of coronary circulation. -tomography-and-angioscopy-ofcoronary-circulation. Published 1/28/2014. Updated January 2015. Accessed February 15, 2015. Variant angina. Published unknown. Updated February 2015. Accessed February 15, 2015. Gaetano AL, Giulia C, Filippo C. Mechanisms of coronary artery

spasm. Circulation. 2011;124:1774-1782. Looi KL, Grace A, Agarwal S. Coronary artery spasm and ventricular arrhythmias. Postgrad Med Journal. 2012;88:465-471.

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