This document discusses criteria for diagnosing myocardial infarction and risk stratification of STEMI patients. It outlines the definition of MI, criteria for acute/evolving MI, and criteria for established MI. It also discusses risk stratification tools like TIMI risk score and management of STEMI in the initial presentation, in-hospital course, and at discharge. Medical management includes oxygen, nitrates, analgesics, and beta blockers. Fibrinolytic therapy and anticoagulation are also summarized.
Based on the principle that the distal coronary pressure measured during vasodilation is directly proportional to maximum vasodilated perfusion.
FFR is defined as the ratio of maximum blood flow in a stenotic artery to maximum blood flow in the same artery if there were no stenosis.
FFR is simply calculated as a ratio of mean pressure distal to a stenosis (Pd) to the mean pressure proximal stenosis, that is the mean pressure in the aorta (Pa), during maximal hyperaemia.
Based on the principle that the distal coronary pressure measured during vasodilation is directly proportional to maximum vasodilated perfusion.
FFR is defined as the ratio of maximum blood flow in a stenotic artery to maximum blood flow in the same artery if there were no stenosis.
FFR is simply calculated as a ratio of mean pressure distal to a stenosis (Pd) to the mean pressure proximal stenosis, that is the mean pressure in the aorta (Pa), during maximal hyperaemia.
HCM is a common genetic heart disease reported in populations globally
Inherited in an autosomal dominant pattern
The distribution of HCM is equal by sex, although women are diagnosed less commonly than men
The prevalence of unexplained asymptomatic hypertrophy in young adults has been reported to range from 1:200 to 1:500
Ventricular tachycardia are difficult to understand. it is classified in to two types. 1. VT in structurally normal heart, 2. VT in heart with structural diseases. I have tried to simplify the VT in structurally normal heart, which may be helpful to many students and learners.
Although the risks of coronary angiography have declined over the years by increased clinical experience and advanced technologies, it still requires attention, knowledge and experience due to being an interventional diagnostic method. A safe coronary angiography begins with the selection of the appropriate catheter for the anatomical structure of the patient and the evaluation of the pressure when the catheter is placed in the coronary ostium. Coronary pressure waves are complementary requirements of angiography. The recognition, evaluation and precautions to be taken for abnormal pressure waves directly affect the mortality of the patient. One of the first clues to the presence of stenosis in the left main coronary artery (LMCA) is abnormal changes in pressure when the catheter is seated in the ostial LMCA. This often occurs as a “ventricularization” or “damping”. For decades, ventricularization was mostly experienced as a stenosis by invasive cardiologists [1]. Recognition of abnormal changes in pressure and precautions to be taken prevent catastrophic outcomes in patients
https://crimsonpublishers.com/ojchd/fulltext/OJCHD.000518.pdf
For more open access journals in Crimson Publishers
please click on https://crimsonpublishers.com/
For more articles in open journal of Cardiology & Heart Diseases
please click on https://crimsonpublishers.com/ojchd/
Pradeep Srivastava Cardiologist is board certified in Internal Medicine, Cardiology and Interventional Cardiology. He completed his Cardiology Fellowship at George Washington University and did his Internal Medicine training at SUNY, University at Buffalo School of Medicine.
HCM is a common genetic heart disease reported in populations globally
Inherited in an autosomal dominant pattern
The distribution of HCM is equal by sex, although women are diagnosed less commonly than men
The prevalence of unexplained asymptomatic hypertrophy in young adults has been reported to range from 1:200 to 1:500
Ventricular tachycardia are difficult to understand. it is classified in to two types. 1. VT in structurally normal heart, 2. VT in heart with structural diseases. I have tried to simplify the VT in structurally normal heart, which may be helpful to many students and learners.
Although the risks of coronary angiography have declined over the years by increased clinical experience and advanced technologies, it still requires attention, knowledge and experience due to being an interventional diagnostic method. A safe coronary angiography begins with the selection of the appropriate catheter for the anatomical structure of the patient and the evaluation of the pressure when the catheter is placed in the coronary ostium. Coronary pressure waves are complementary requirements of angiography. The recognition, evaluation and precautions to be taken for abnormal pressure waves directly affect the mortality of the patient. One of the first clues to the presence of stenosis in the left main coronary artery (LMCA) is abnormal changes in pressure when the catheter is seated in the ostial LMCA. This often occurs as a “ventricularization” or “damping”. For decades, ventricularization was mostly experienced as a stenosis by invasive cardiologists [1]. Recognition of abnormal changes in pressure and precautions to be taken prevent catastrophic outcomes in patients
https://crimsonpublishers.com/ojchd/fulltext/OJCHD.000518.pdf
For more open access journals in Crimson Publishers
please click on https://crimsonpublishers.com/
For more articles in open journal of Cardiology & Heart Diseases
please click on https://crimsonpublishers.com/ojchd/
Pradeep Srivastava Cardiologist is board certified in Internal Medicine, Cardiology and Interventional Cardiology. He completed his Cardiology Fellowship at George Washington University and did his Internal Medicine training at SUNY, University at Buffalo School of Medicine.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
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2 Case Reports of Gastric Ultrasound
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
2. Definition of MI
Risk stratification
Medical management
3. (Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of
Cardiology committee for the redefinition of myocardial infarction:. J. Am. Coll. Cardiol. 2000;36;959-969)
Criteria for Acute, Evolving, or Recent MI
Either of the following criteria satisfies
1. Typical rise &/or fall of biochemical markers of myocardial
necrosiswith at least one of the following:
a) Ischemic symptoms
b) ECG changes indicative of new ischemia (new ST elevation or
new/presumed to be new LBBB)
c) Development of pathological Q waves in the ECG
d) Imaging e/o new loss of viable myocardium or new RWMA
2. Pathologic findings of an acute MI
4. (Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of
Cardiology committee for the redefinition of myocardial infarction:. J. Am. Coll. Cardiol. 2000;36;959-969)
PCI periprocedural MI:
increases of biomarkers >3 x 99th percentile URL
CABG-related MI
Increases of biomarkers >5 x 99th percentile URL
plus either new pathological Q waves or new LBBB,
or angiographically documented new graft or native
coronary artery occlusion, or imaging evidence of
new loss of viable myocardium.
5. (Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of
Cardiology committee for the redefinition of myocardial infarction:. J. Am. Coll. Cardiol. 2000;36;959-969)
Criteria for established MI.
Either of the following criteria satisfies
1. Development of new pathologic Q waves on serial ECGs.
The patient may or may not remember previous
symptoms. Biochemical markers of myocardial necrosis
may have normalized, depending on the length of time
that has passed since the infarct developed.
2. Pathologic findings of a healed or healing MI.
6.
7. There is risk stratification within STEMI,
but in general, STEMI is high-risk
Important to select greater-risk patients
who warrant more aggressive strategies
for prevention of future serious events
such as reinfarction or sudden death
8. Occurs in several stages
Initial presentation
In-hospital course (CCU, intermediate CU)
At the time of hospital discharge
9. Prior angina
pectoris
Prior MI
Female gender
Hypertension
History of CHF
Hyperlipidemia
Diabetes
ECG Criteria
Markedly elevated
cardiac enzymes
Elevated BUN
Complications
VSR/PMD-rupture
Myocardial rupture
10. Anterior MI/ Persisting ST elevation
Q waves in multiple leads
RVMI + IWMI
High sum of ST elevation
Reciprocal ( anterior ) ST depression
Persisting ST depression
Prolonged QT
Conduction defects/ heart block
Sinus tachycardia/atrial fibrillation
11. Killip Classification % patients Mortality (%)
I No CHF 30-50 5
II Rales, S3, Pulmonary venous hypertension 33 15-20
III Pulmonary edema 15 40
IV Cardiogenic shock 10 80-100
(Killip T, and Kimball JT: Treatment of myocardial infarction in a coronary care unit: a two year
experience of 250 patients. American Journal of Cardiology 1967; 20: 457-464 )
Left ventricular dysfunction is the single most important predictor of mortality
12. TIMI
GRACE
PURSUIT
ACI-TIPI
Goldman
best used to supplement—not replace—
clinical judgment
less useful in atypical presentations, but
indeed validated in an ED population . . .
13. (David A et al. TIMI Risk Score for ………..: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy.
Circulation 2000, 102:2031-2037)
14. (David A et al. TIMI Risk Score for ………..: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy.
Circulation 2000, 102:2031-2037)
15. ( Wiviott SD et al Performance of the TRI in the National Registry of Myocardial Infarction-3 and -4:. J Am Coll Cardiol
2004;44:783–9 )
Derived from In TIME II trial & validated in TIMI-9
trials
Based on age and vital signs, in predicting mortality
among a large, community based, unselected,
heterogeneous population
Heart rate [age/10 ]2 /systolic blood pressure
A strong and independent predictor of mortality at
24 h and at 30 days (p 0.0001)
16.
17. Can be used to predict the cumulative risk of
death and death or myocardial infarction in
the period from admission to hospital to six
months after discharge
The tool is simple and applicable to patients
across the complete spectrum of acute
coronary syndrome
18.
19. Exercise Testing
performed either in the hospital or early after discharge in
patients not selected for cardiac catheterization and
without high-risk features to assess the presence and
extent of inducible ischemia Class I (B)
Exercise testing might be considered before discharge of
patients recovering from STEMI to guide the post discharge
exercise prescription or to evaluate the functional
significance of a coronary lesion previously identified at
angiography Class IIb (C)
20. Sub maximal protocol
Target workload =5 METS, 70 % MPHR or symptom
limited
Predictors of poor outcome
Ischemic ST depression > 1 mm is inconsistent
predictor of mortality
poor exercise tolerance < 3 minutes doubles one
year mortality ( 7% to14%)
Inability to exercise or contra-indication to TMT
identifies High Risk patient.
21. Late Risk Stratification - 4 to 8 weeks
(Assessment of residual ischaemia)
TMT
Stress echocardiography
Adenosine/Dipyridamole Perfusion imaging
Un-interpretable ECG
Equivocal TMT
Inability to exercise
22.
23. Prehospital EMS providers …162 to 325 mg
of aspirin (chewed) …non–enteric-coated
formulations.
(goal is to quickly block thromboxane A2 formation in platelets)
Previously on NTG take I tab S/L Not
improving after 5 mts Seek medical help
24. EMS Transport
Onset of
symptoms of
STEMI
EMS
Dispatch
EMS on-scene
• Encourage 12-lead ECGs.
• Consider prehospital fibrinolytic if
capable and EMS-to-needle within
30 min.
GOALS
PCI
capable
Not PCI
capable
Hospital fibrinolysis:
Door-to-Needle
within 30 min.
Inter-
Hospital
Transfer
Golden Hour = first 60 min. Total ischemic time: within 120 min.
Patient EMS Prehospital fibrinolysis
EMS-to-needle
within 30 min.
EMS transport
EMS-to-balloon within 90 min.
Patient self-transport
Hospital door-to-balloon
within 90 min.
Dispatch
1 min.
5
min.
8
min.
25. Early presentation (≤3 hr from symptom onset and
delay to invasive strategy)
Invasive strategy is not an option
Catheterization laboratory occupied or not available
Vascular access difficulties
Lack of access to a skilled PCI laboratory
Delay to invasive strategy
Prolonged transport
(Door-to-balloon)–(door-to-needle) more than 1 hr
Medical contact-to-balloon or door-to-balloon more
than90 min
26. Skilled PCI laboratory is available with surgical backup
Medical contact-to-balloon or door-to-balloon
less than 90 min
High risk from STEMI
Cardiogenic shock
Killip class ≥ 3
Contraindications to fibrinolysis
Late presentation (> 3 hr)
Diagnosis of STEMI is in doubt
27. 1. Airway, Breathing, Circulation (ABC)
2. Vital signs, general observation
3. Presence or absence of jugular venous
distension
4. Pulmonary auscultation for rales
5. Cardiac auscultation for murmurs and
gallops
6. Presence or absence of stroke
28. should be performed, but should not delay the
implementation of reperfusion therapy.
Serum biomarkers for cardiac damage
Complete blood count (CBC) with platelets
International normalized ratio (INR)
Activated partial thromboplastin time (aPTT)
Electrolytes and magnesium
Blood urea nitrogen (BUN),creatinine
Glucose
Complete Lipid Profile
29. 0 1 2 3 4 5 6 7 8
Cardiac troponin-no reperfusion
Days After Onset of STEMI
MultiplesoftheURL
Upper reference limit
1
2
5
10
20
50
URL = 99th %tile of
Reference Control Group
100
Cardiac troponin-reperfusion
CKMB- reperfusion
CKMB- no reperfusion
30. Pain contribute to the heightened sympathetic
activity
Typically accomplished with combination of
nitrates, analgesics, oxygen and β-blockers
Oxygen
Arterial oxygen desaturation (SaO2 < 90%) Class I(B)
Uncomplicated STEMI during the first 6 hours Class II(A)
31. Nitroglycerin Class I (C)
Patients with ongoing ischemic discomfort
0.4 mg every 5 minutes for a total of 3 doses
Intravenous NTG
Ongoing ischemic discomfort that responds to nitrate therapy
control of hypertension
management of pulmonary congestion.
Nitrates should not be administered to patients with:
systolic pressure < 90 mm Hg or ≥ to 30 mm Hg below baseline
severe bradycardia (< 50 bpm)
tachycardia (> 100 bpm)
suspected RV infarction.
who have received a phosphodiesterase
32. Analgesia
Morphine sulfate (2 to 4 mg intravenously)Class I (C)
NSAIDS Increase risk of cardiovascular events so should be discontinued
[A sub study analysis from the ExTRACT TIMI-25 trial showed increased risk
of death, reinfarction, heart failure, or shock among patients on NSAIDs
within 7 days of enrollment].
Aspirin
Should be chewed by patients who have not taken aspirin
before presentation with STEMI. The initial dose should
be 162 mg Class I (A) to 325 mg. Class I (C)
33. The principal goal of fibrinolysis is prompt restoration
of full IRA patency
Streptokinase , tPA,, TNK, rPA
TNK and rPA - bolus fibrinolytics
Promote conversion of plasminogen to plasmin, which
subsequently lyses fibrin thrombi
34.
35.
36. Absolute Contraindications:
Any prior intracranial hemorrhage
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischemic stroke within 3 months EXCEPT acute ischemic
stroke within 3 hours
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed-head or facial trauma within 3 months
Note: Age restriction for fibrinolysis has been removed compared with prior
guidelines.
37. Relative Contraindications:
Severe uncontrolled hypertension on presentation (SBP > 180
or DBP > 110)
Prior ischemic stroke >3 months
Traumatic or prolonged (> 10 mt.) CPR or major surgery (< 3
weeks)
Recent (< 2 to 4 weeks) internal bleeding
Noncompressible vascular punctures
For streptokinase/anistreplase: prior exposure (> 5 days ago)
or prior allergic reaction to these agents
Pregnancy, Active peptic ulcer
Current use of anticoagulants
38. (Antman EM et al: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. Circulation
110:e82, 2004.)
PARAMETER STREPTOKINASE ALTEPLASE RETEPLASE TNK t-PA
Dose 1.5 MU in 30-60 min
Up to 100 mg in
90 min (based on
weight)
10 U ? 2 (30 min
apart) each over
2 min
30-50 mg
based on
weight
Bolus administration No No Yes Yes
Antigenic Yes No No No
Allergic reactions
hypotension most
common
Yes No No No
Systemic fibrinogen
depletion
Marked Mild Moderate Minimal
90-min patency rates
(%)
≈50 ≈75 ≈75 ≈75
TIMI grade 3 flow (%) 32 54 60 63
Cost per dose (Rs) 2500 39375 (50mg)
39. WP-4 hr. t-PA is the preferred treatment
streptokinase t-PA equivalent choices -risk of
death is low , and increased risk of ICH .
WP-4 to 12 hr . streptokinase and t-PA are
equivalent options, but streptokinase is
probably preferable to t-PA because of cost
considerations
40. LATE and EMERAS trials
Fibrinolytics between 12 and 24 hours
No mortality benefit
Increases risk of cardiac rupture
41. Noninvasive findings s/o reperfusion include:
Relief of symptoms
Maintenance and restoration of hemodynamic
and/or electrical instability
Reduction of ≥ 50% of the initial STE pattern on
follow-up ECG 60 to 90 minutes after initiation of
therapy.
Class II(A)
42. Flow in the IRA angiographically
Gd. 0, compl. Occlussion
Gd. 1, some penetration
Gd.2, entire vessel with
Impaired flow
Gd.3, entire vessel with
Normal flow
43. Prevention of DVT, pulmonary embolism,
ventricular thrombus, cerebral embolization.
Establishing & maintaining patency of IRA.
Trials shown that more prolonged anticoagulant
therapy is beneficial (duration of index hospita-
lization) in patients receiving thrombolytic
therapay
44.
45. IV Unfractionated Heparin
Selective Fibrinolytic – Bolus of 60 U/kg (maximum 4000 U)
followed by an infusion of 12 U/kg/hr (maximum 1000 U)
(Level of Evidence: C)
Nonselective fibrinolytic agents- who are at high risk for
systemic emboli (large or anterior MI, atrial fibrillation (AF),
previous embolus, or known LV thrombus).
(Level of Evidence: B)
LMWH- 30mg iv followed by 1mg/kg every 12hr.
46. Aspirin should be given indefinitely to all STEMI
pts. without a true aspirin allergy.
Class I (A)
Patients undergoing PCI are also given aspirin
loading
Class I (B)
Patients not on aspirin therapy should be given
nonenteric aspirin 325 mg before PCI.
Class I(B)
After PCI, use of aspirin should be continued
indefinitely
Class I (A)
47. Addition of P2Y12 inhibitor to aspirin warranted for most
patients with STEMI (COMMIT & CLARITY-TIMI22)
In patients for whom PCI is planned, clopidogrel should
be started and continued: Class I (B)
Patients receiving a stent (BMS or DES) clopidogrel 75 mg daily
or prasugrel 10 mg for at least 12 months;
If the risk of bleeding outweighs the anticipated benefit
afforded by thienopyridine therapy, earlier discontinuation .
Continuation of thienopyridines beyond 15 months may
be considered in patients undergoing DES placement
48. Prior history of stroke and TIA for whom primary PCI is
planned, prasugrel is not recommended
CABG planned ?... the drug should be withheld for at
least 5 days in patients receiving clopidogrel and at
least 7 days in patients receiving prasugrel, Class I (B)
Probably indicated in patients receiving fibrinolytic
therapy who are unable to take aspirin because of
hypersensitivity or GI intolerance Class I (C)
49. It is reasonable to start abciximab as early as
possible before primary PCI (with or without
stenting) in patients with STEMI.
Tirofiban or eptifibatide may be considered
before primary PCI (with or without stenting)
in patients with STEMI.
50. Relieve ischemic pain, reduce need for analgesics,
reduce infarct size and life-threatening arrhythmias
Contra indications:
signs of heart failure
evidence of a low output state
increased risk for cardiogenic shock
other relative contraindications (PR interval > 0.24 S. 2nd or
3rd degree AV block, or reactive airway disease)
51.
52. Favorable effects with metoprolol, atenolol,
carvedilol and timolol,
Beta blockers with intrinsic sympathomimetic
activity probably should not be chosen.
Trial of esmolol in the presence of relative
contraindications.
53. Favorable impact on ventricular remodeling,
improvement in hemodynamics, and
reductions in congestive heart failure
Angiotensin-converting enzyme inhibitors
Angiotensin II receptor blockers
Aldosterone blockade
54.
55.
56.
57.
58. EPHESUS trial: Eplerenone, 25 mg/day titrated to
50 mg/day for high-risk patients following STEMI (EF
≤40%, clinical HF, DM)
Mean follow-up 16 months, there was a 15% reduction in
the RR of mortality
59. Immediate-release preparation of nifedipine increased
risk of in-hospital mortality
Verapamil & diltiazem can be given for relief of
ongoing ischemia or slowing of a rapid ventricular
response in AF in patients with contraindication to
beta blockers.
INTERCEPT trial compared 300 mg of diltiazem with
placebo and Diltiazem did not reduce cardiac death,
nonfatal reinfarction, during a 6-month follow-up
60. It is reasonable to use an insulin based regimen to
achieve and maintain glucose levels less than 180
mg/dl while avoiding hypoglycemia for patients
with STEMI with either a complicated or
uncomplicated course Class IIa(B)
61. In the absence of complications patients need
not be confined to bed for more than 12 hours
Progression of activity should be individualized
62. first day and as late as 6 weeks after STEMI
Radiation of the pain to either trapezius ridge.
Treatment consists of aspirin doses of 650 mg
orally every 4 to 6 hours may be necessary.
NSAIDs and steroids should be avoided
63. Anticoagulation- heparin to elevate the aPTT to
1.5 to 2 times that of control, followed by a
minimum of 3 to 6 months of warfarin in the
following clinical situations:
An embolic event has already occurred or
The patient has a large anterior infarction whether or
not a thrombus is visualized echocardiographically
64. More in older patients, women , hypertensive
More frequently in the left than right ventricle
1 day and 3 weeks, most commonly 1 to 4 days
Near the junction of infarct and normal muscle
Most often in patients without previous infarcts
Fibrinolytic therapy more than PCI
65. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT
THERAPEUTIC
OPTIONS
Electrical
instability
Ventricular
premature beats
Correction of electrolyte deficits and
increased sympathetic tone
Potassium and
magnesium solutions,
beta blocker
Ventricular
tachycardia
Prophylaxis against ventricular
fibrillation, restoration of
hemodynamic stability
Antiarrhythmic agents;
cardioversion/defibrillatio
n
Ventricular
fibrillation
Urgent reversion to sinus rhythm
Defibrillation; bretylium
tosylate
Accelerated
idioventricular
rhythm
Observation unless hemodynamic
function is compromised
Increase sinus rate
(atropine, atrial pacing);
antiarrhythmic agents
Nonparoxysmal
atrioventricular
junctional
tachycardia
Search for precipitating causes (e.g.,
digitalis intoxication); suppress
arrhythmia only if hemodynamic
function is compromised
Atrial overdrive pacing;
antiarrhythmic agents;
cardioversion relatively
contraindicated if digitalis
intoxication present
67. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT
THERAPEUTIC
OPTIONS
Bradyarrhyth
mias and
conduction
disturbances
Sinus
bradycardia
Acceleration of heart rate only
if hemodynamic function is
compromised
Atropine; atrial pacing
Junctional escape
rhythm
Acceleration of sinus rate only
if loss of atrial “kick” causes
hemodynamic compromise
Atropine; atrial pacing
Atrioventricular
block and
intraventricular
block
Insertion of pacemaker
68.
69.
70.
71. At time of discharge patient should be on:
ASA unless contra-indication
Clopidogrel if PCI/NSTEMI (duration minimum1 year)
Longer duration of clopidogrel if DES in critical location or
complex lesion
-blocker unless contra-indication
ACE inhibitor for CHF or LV dysfunction
All for vascular protection?
Statin for LDL to < 70mg%(minimum 50% reduction)
72. High Risk
extensive ECG changes
anterior/ infero-posterior/
prior MI
Residual ischaemia
post MI angina
positive TMT/ perfusion
scan
non-Q MI
ischaemia at a distance
Complicated MI
CHF/ flash pulmonary
edema
shock
heart block
RBBB
sustained ventricular
arrhythmias
Anxiety/ physical
labor/ young age
73.
74. Smoking Goal: Complete Cessation
With in 2yrs risk of nonfatal MI falls to normal
Blood pressure control:
Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic
kidney disease or diabetes
Physical activity:
Minimum goal: 30 minutes 3 to 4 days per week; Optimal
daily
75. Weight management:
Goal: BMI 18.5 to 24.9 kg/m2
Waist circumference: Women < 35 in. Men: < 40 in.
Diabetes management:
Goal: HbA1c < 7%
Lipid management: Primary goal: LDL-C <70mg%
Start dietary therapy in all patients (< 7% of total calories as
saturated fat and < 200 mg/d cholesterol). Promote physical activity
and weight management. Encourage increased consumption of
omega-3 fatty acids.
Assess fasting lipid profile in all patients, preferably within 24 hours
of STEMI. Add drug therapy according to the following guide:
76. LDL-C < 100 mg/dL (baseline or on treatment):
Statins should be used to lower LDL-C.
LDL-C ≥ 100 mg/dL (baseline or on treatment):
Intensify LDL-C–lowering therapy with drug treatment, giving preference to statins.
If TGs are ≥ 150 mg/dL or HDL-C is < 40 mg/dL:
Emphasize weight management and physical activity. Advise smoking cessation.
If TG is 200 to 499 mg/dL:
After LDL-C–lowering therapy, consider adding fibrate or niacin.
If TG is ≥ 500 mg/dL:
Consider fibrate or niacin before LDL-C–lowering therapy.
Consider omega-3 fatty acids as adjunct for high TG.
77. Hormone therapy:
with estrogen plus progestin should not be given de novo to postmenopausal
women after STEMI for secondary prevention of coronary events. Class III (A)
Postmenopausal women who are already taking estrogen plus progestin at the
time of STEMI should not continue hormone therapy. Class II (B)
However, women who are beyond 1 to 2 years after initiation of hormone
therapy who wish to continue such therapy for another compelling indication
should weigh the risks and benefits. Class III (A)
Antioxidant vitamins:
such as vitamin E and/or vitamin C supplements should not be prescribed to
patients recovering from STEMI to prevent cardiovascular disease
78. Psychosocial status of the patient should be evaluated,
including inquiries regarding symptoms of depression,
anxiety, or sleep disorders and the social support
environment. Class I (C)
Treatment with cognitive-behavioral therapy and selective
serotonin reuptake inhibitors can be useful for STEMI
patients with depression that occurs in the year after
hospital discharge. Class IIa (A)
79. RRR 2yr Event Rate
None 8%
ASA 25% 6%
-Blockers 25% 4.5%
Lipid lowering 30% 3.0%
ACE-
inhibitors
25% 2.3%
( Yusuf, S. Two decades of progress in preventing vascular disease. Lancet 2002; 360: 2-3).
Cumulative relative risk reduction if all four drugs are used is about 75%