Transcript NSTEMI by Rainier Tanalgo

Fixing A Broken Heart!
DEPARTMENT OF
INTERNAL MEDICINE
1. To present a case of 71yo patient who had difficulty of
breathing after diving.
2. To present a case of a patient presented with NSTEMI
with normal coronary angiographic findings.
1 Day PTA
Deep sea diving (70 feet)
Panicked/ anxiety attack
Difficulty of breathing
(+) chest tightness, (+) nausea, (+) dizziness, (-)
epigastric pain, (-) nausea, (-) vomiting
ADMISSION
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No history of headaches, dizziness
No cough, fever, chest pain
No weight loss, edema
No abdominal pains, no urinary and bowel movement
changes, no joint pains, no pruritus, no numbness
No sensorial changes, behavioral changes, visual
changes, seizures, focal weekness, easy fatigability, no
hearing loss
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(+) Hypothyroid and maintained on unrecalled medication
(+) Depression treated since the 1980’s
(+) Vaginal hysterectomy
(+) Shingles in 2004
(+) Bilateral bunionectomy
(+) Sclerotherapy for varicose veins of the lower extremities
(+) Allergic to Penicillins- itchiness
(-) Hypertension
(-) Diabetes mellitus
(-) Bronchial asthma.
(+) Hypertension
(+) Coronary Artery Disease
(+) Dyslipidemia
(+) Thyroid disease
rBoth parents
sides
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Non-smoker
Occasional alcoholic beverage drinker
Conscious, coherent, oriented, not in distress:
BP=106/72mmHg
HR=82bpm
RR=20cpm
Temp=37C O2 Sat 93% at 4LPM nasal cannula
Ht: 167.64 cm
Wt: 68kgs BMI: 24.19 kg/M2
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Skin: warm, good turgor, no pallor, no cyanosis, no skin
color changes
HEENT: anicteric sclera, pinkish palpebral conjunctivae, no
naso-aural discharges, no tonsilopharyngeal congestion,
Neck: no neck vein distention, JVP=5-6cm, no
lymphadenopathy, non-palpable thyroid gland, no carotid
bruit
Chest and Lungs: no retractions, symmetrical chest
expansion, mid to base bilateral coarse rales, no
wheezing
 Heart: normal rate, regular rhythm, apex beat at 5th
ICS LMCL, S1>S2 at apex, S2>S1 at base, no S3, no
heave, no thrill, no murmur
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Abdomen: flat, normoactive bowel sounds, soft, nontender, no organomegaly, no masses
Extremities: no edema, left leg noted slightly bigger than
right leg (reportedly fell 3 weeks ago and injured left knee)
Subjective Findings
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71/Female
Difficulty of breathing after diving
Elevate d Trop I
Pulmonary edema on CXR
Bilateral crackles from mid to base
Objective findings
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Bilateral crackles from mid to
base
Normal vital signs
Patient
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71/Female
Difficulty of breathing after diving
Difficulty of breathing after diving
Elevate d Trop I
Pulmonary edema on CXR
Bilateral crackles from mid to base
Non ST Elevation Myocardial
Infarction
•Chest pain described as a pressure
sensation, fullness, or squeezing in the
midportion of the thorax
•Radiation of chest pain into the jaw or
teeth, shoulder, arm, and/or back
•Associated dyspnea or shortness of
breath
•Associated epigastric discomfort with or
without nausea and vomiting
•Associated diaphoresis or sweating
•Syncope or near syncope without other
cause
•Impairment of cognitive function without
other cause
Patient
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71/Female
Difficulty of breathing
after diving
Elevate d Trop I
Pulmonary edema on
CXR
Bilateral crackles from
mid to base
ECG: Non specific ST
wave chenges
Decompression sickness
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Extreme Fatigue, Pain in Joints, Muscle Pain,
Dizziness, Paralysis, Rash on Skin, Staggering,
Choking. Decreased Sensation, Collapse or
Unconsciousness
P wave peaking and P-R depression compatible
with right heart strain; S-T segment and T wave
changes suggestive of myocardial ischemia; and
ventricular arrhythmias ranging from unifocal
premature
ventricular
contractions
to
ventricular tachycardia
Patient
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Acute Pulmonary Embolism
Most common symptom is
71/Female
Difficulty of breathing after diving unexplained shortness of breath
and/or chest pain with difficulty
Elevate d Trop I
breathing
Pulmonary edema on CXR
Chest pain, often worse when taking a
Bilateral crackles from mid to base breath
A feeling of apprehension
Sudden collapse
Coughing
Sweating
Non-specific ST changes
Tachycardia
Acute pulmonary edema probably secondary to Acute
Coronary Syndrome-Non ST elevation Myocardial
Infarction
Rule out Decompression Sickness
Rule out Acute Pulmonary Embolism
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Patient started on MI protocol (Enoxaparin, ASA,
Clopidogrel, Bromazepam and Lactulose,
Furosemide,and Rosuvastatin
ECG showed non-specific ST-T wave changes, poor R
wave progression
Electrolytes
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CXR: There are no active parenchymal infiltrates seen.
Pulmonary vessels are within normal limits.
Heart is normal in size and configuration.
Mediastinum, diaphragm, and bony thorax are
unremarkable.
ABG: Respiratory alkalosis
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Cardiac enzymes were elevated (Trop I 10.62 ng/ml,
CPK 732 U/L and CPK MB isoenzyme 40.40 ng/ml).
Pro BNP and D dimer were elevated
Protime was normal
CBC showed leukocytosis (WBC 13.25) with
predominance of segmenters(80) and monocytes(10)
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2 D echo revealed dilated left ventricular dimensions
with left ventricular global hypokinesia; LVEF of 36%
by Teicholz and 35% by Simpson’s. MR, mild. TR, mild.
Second Hopsital Day
 Repet ECG: Sinus tachycardia with occasional
premature ventricular contraction
 Patient had hypotension
 Inotropes started with Dopamine and Dobutamine
 Patient was scheduled for stat left heart
catheterization with coronary angiography on double
set up for possible angioplasty and CABG
Second Hopsital Day
 Repeat cardiac enzymes: Trop I 4.42, CPK 374, CPK MB
isoenzyme 15.90
 Electrolytes
Second Hopsital Day
Left heart catheterization with coronary angiography:
Conclusion: Minimal, nonobstructive,
atherosclerotic coronary artery disease.
 Markedly elevated LVEDP at rest.
 The etiology of the LV systolic dysfunction noted on
2 D echocardiography and elevation of cardiac
markers is uncertain.
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Fourth Hopsital Day
Repeat 2 D echo:NLVD with hypokinesia of the
anterior interventricular septum and anterior
and lateral LV wall from base to apex. LVEF
54% by Teicholz and 54% by Simpson’s.
Normal left and right atria. Normal right
ventricle. Normal main pulmonary artery and
aortic root dimensions. Calcification on aortic
walls. Mitral and aortic annular calcification.
Fourth Hopsital Day
Repeat 2 D echo:
 Color flow and Doppler study: MR, trivial. TR, trivial.
Calculated pulmonary artery pressure by TR jet 40
mmHg. Pulmonary hypertension, mild.
 Compared with previous study done Jan. 15, 201103-10
 Left ventricular end diastolic diameter decrease
from 5.4cm to 4.7cm.
 Ejection fraction has increase from 36% to 54%.
Fourth Hopsital Day
 Venous dupplez scan of lower extremities: Normal
 Carotid doppler: Normal
Fifth Hopsital Day
 Patient was stable
 Transferred out to regular room
 Referred to cardiac rehab
 Discaharged on the 8th hospital day
 CXR
Follow after 1 month
Trans esophangeal echocardiogram performed
LV: normal LV chamber size. NLVSF. ELVEF, 65%.
No regional wall motion abnormalities. NRVSF.
No shunt at atria level by color flow imaging and
agitated contrast injection
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71/F
Sudden dyspnea after diving
Non-specific ST changes
Elevated cardiac enzymes
2 D echo with segmental wall hypokinesia with
improvement after 4 days
Normal Coronary angiogram
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Acute Cornary Syndrome- Non ST Elevation
Myocardial Infarction complicated by pulmonary
edema
Tako-Tsubo cardiomyopathy
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Tako-Tsubo – Japanese name for octopus trap
fisherman uses to catch octopus.
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TTC – Heart (LV)
 Like the shape of an octopus trap
Other names:
Stress induced cardiomyopathy
Transient LV apical balooning
Apical balooning syndrome
Tako-Tsubo Cardiomyopathy
An antique tako-tsubo.
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Early 1990’s – 1st reported in Japan by Sato et al
Early 2000 – recognized in western white
population, Africans, Americans, Asians
High prevalence in Japan
Women : men ratio (7:1)
Age
 68.6 + 12.2 women
 65.9 + 9.1 men
Kinji Ishikawa, M.D.
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TTC accounts for 2% of all patients presenting
with CP and ST elevation.
Gianni et al
European Heart Journal 2006
27: 1523-1529
• Transient, reversible akinesis or dyskinesis of the left
ventricular apical and mid-ventricular segments with
regional wall motion abnormalities extending beyond a
single vascular territory on left ventriculography.
• Absence of obstructive coronary artery stenosis > 50% of
the luminal diameter or angiographic evidence of acute
plaque rupture.
MJA • Volume 187 Number 6 • 17 September 2007
• New electrocardiographic abnormalities consisting of ST-
segment elevation or T-wave inversion.
• Absence of:recent head trauma, intracranial bleeding,
phaeochromocytoma, obstructive epicardial coronary
artery disease, myocarditis, hypertrophic cardiomyopathy
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Exact mechanism unknown
Evidences point to:
 Catecholamine mediated mechanism via cardiac
sympathetic neurons which can be triggered by
emotional or physical stress.
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 Myocardial stunning form multiple site microvascular
spasm
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Wall motion localized at the distal half of the LV
(apical balooning)
 More dense adrenoreceptors at the apex.
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Stressors
 65 – 80% - with identifiable stressors
 50% - emotion
 50% - physical
 20 – 35% – non identified
Irfran Abdulla, MD
Clinical Update
MJA vol 187 No. 6 – 17 Sept 07
• Unexpected death in the family
• Gambling and financial losses
• Devastating medical diagnosis
• Car accidents
• Public speaking
• Earthquakes
• Acute physical trauma
• Robbery
• Major surgical procedures
MJA • Volume 187 Number 6 • 17 September 2007
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FIGURE 1. Different end-systolic left ventricular (LV) silhouettes published in
different articles under the term “Takotsubo syndrome” (transient LV apical
ballooning or broken heart syndrome). The tracing was done exactly over the
shape of the angiograms from the articles (A, Abe et al8; B, San Roman Sanchez et
al9; C, Wittstein et al10; D, Rivera et al3; E, Desmet et al11; and F, Reyburn and
Vaglio4). As can be clearly seen, there is wide heterogeneity among the different
patterns, varying from a relatively small akinetic apical area in C to a wide global
akinesia in D and E.
Mayo Clin Proc. • June 2006;81(6):732-735 •
www.mayoclinicproceedings.com
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Post menopausal – female
Chest pain, dyspnea, hypotension
1-5% hemodynamically unstable
ECG – ST elevation in V3 – V6 or diffuse ST – T
changes
Troponin & CK-MB – no rise or min 
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Serum nor epinephrine – significantly 
LV wall motion – apical balooning or dyskinesia
and basal hyperkinesia during systole
Coronary Angio – no significant CAD
Precipitating factors – severe emotional or
physical stress
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Self – limiting disorder
 – Blocker
ACE I
Caution on patients
 With LVOT obstruction
 Avoid
 Inotropes
 Volume depletion
 Vasodilators
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Excellent despite
 Hemodynamic compromise in some patients
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Hospital mortality 0 – 8%
LV systolic function (N) in 1 – 4 weeks
Recurrent rate low 1 – 5%
Long term Rx – unclear
1. Is a reversible cardiomyopathy triggered
by psychologically stressful events.
2. Occurs in older women and may mimic
evolving acute myocardial infarction or
coronary syndrome.
3. Must be taken into consideration
regardless the geographical area.
4. The complete explorations
(echocardiography, angiography, MRI
and myocardial scintigraphy) contribute
to a better and more complete
diagnosis and are important for
evolution, consequences and
ppropriate medical therapy.
Thank you very much
Jan. 18, 2011
ECG
1/14/2 Non specific ST wave changes.
Poor R wave progression.
011
1154H
1/15/2 Sinus tachycardia with occasional
011
premature ventricular
0535H contraction