Primary PCI involves performing urgent angioplasty and potentially stenting of the culprit artery in STEMI patients, with the goal of reopening the blocked vessel within 90 minutes of first medical contact. It is the preferred reperfusion strategy when it can be performed promptly by an experienced team. Factors such as patient age, time to treatment, comorbidities, and initial flow in the artery help determine whether primary PCI or thrombolysis is most appropriate. Optimal anticoagulation and antiplatelet regimens along with adjunctive therapies like manual thrombectomy can improve outcomes of primary PCI.
There are many interventional cardiac procedure those need a trans septal puncture of the interatrial septum. This presentation clearly elaborates everything you need to know about the TSP.
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.
There are many interventional cardiac procedure those need a trans septal puncture of the interatrial septum. This presentation clearly elaborates everything you need to know about the TSP.
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.
Wellens syndrome. Wellens syndrome (also referred to as LAD coronary T-wave syndrome) refers to an ECG pattern specific for critical stenosis of the proximal left anterior descending artery. The anomalies described occur in patients with recent anginal chest pain, and do not have chest pain when the ECG is recorded.
Congenital defects can put a strain on the heart, causing it to work harder. To stop your heart from getting weaker with this extra work, your doctor may try to treat you with medications. They are aimed at easing the burden on the heart muscle. You need to control your blood pressure if you have any type of heart problem.
Changing your lifestyle can help control and manage high blood pressure. Your health care provider may recommend that you make lifestyle changes including:
Eating a heart-healthy diet with less salt
Getting regular physical activity
Maintaining a healthy weight or losing weight
Limiting alcohol
Not smoking
Getting 7 to 9 hours of sleep daily
CRISPR technologies have progressed by leaps and bounds over the past decade, not only having a transformative effect on
biomedical research but also yielding new therapies that are poised to enter the clinic. In this review, I give an overview of (i)
the various CRISPR DNA-editing technologies, including standard nuclease gene editing, base editing, prime editing, and epigenome editing, (ii) their impact on cardiovascular basic science research, including animal models, human pluripotent stem
cell models, and functional screens, and (iii) emerging therapeutic applications for patients with cardiovascular diseases, focusing on the examples of Hypercholesterolemia, transthyretin amyloidosis, and Duchenne muscular dystrophy.
A post-splenectomy patient suffers from frequent infections due to capsulated bacteria like Streptococcus
pneumoniae, Hemophilus influenzae, and Neisseria meningitidis despite vaccination because of a lack of
memory B lymphocytes. Pacemaker implantation after splenectomy is less common. Our patient underwent
splenectomy for splenic rupture after a road traffic accident. He developed a complete heart block after
seven years, during which a dual-chamber pacemaker was implanted. However, he was operated on seven
times to treat the complication related to that pacemaker over a period of one year because of various
reasons, which have been shared in this case report. The clinical translation of this interesting observation
is that, though the pacemaker implantation procedure is a well-established procedure, the procedural
outcome is influenced by patient factors like the absence of a spleen, procedural factors like septic measures,
and device factors like the reuse of an already-used pacemaker or leads.
Transcatheter closure of patent ductus arteriosus (PDA) is feasible in low-birth-weight infants. A female baby was born prematurely with a birth weight of 924 g. She had a PDA measuring 3.7 mm. She was dependent on positive pressure ventilation for congestive heart failure in addition to the heart failure medications. She could not be discharged from the hospital even after 79 days of birth, and even though her weight reached 1.9 kg in the neonatal intensive care unit. We attempted to plug the PDA using an Amplatzer Piccolo Occluder, but the device failed to anchor. Then, the PDA was plugged using a 4-6 Amplatzer Duct Occluder using a 6-Fr sheath which was challenging.
Accidental misplacement of the limb lead electrodes is a common cause of ECG abnormality and may simulate pathology such as ectopic atrial rhythm, chamber enlargement or myocardial ischaemia and infarction
A Case of Device Closure of an Eccentric Atrial Septal Defect Using a Large D...Ramachandra Barik
Device closure of an eccentric atrial septal defect can be challenging and needs technical modifications to avoid unnecessary complications. Here, we present a case of a 45-year-old woman who underwent device closure of an eccentric defect with a large device. The patient developed pericardial effusion and left-sided pleural effusion due to injury to the junction of right atrium and superior vena cava because of the malalignment of the delivery sheath and left atrial disc before the device was pulled across the eccentric defect despite releasing the left atrial disc in the left atrium in place of the left pulmonary vein. These two serious complications were managed conservatively with close monitoring of the case during and after the procedure.
Trio of Rheumatic Mitral Stenosis, Right Posterior Septal Accessory Pathway a...Ramachandra Barik
A 57-year-old male presented with recurrent palpitations. He was diagnosed with rheumatic mitral stenosis, right posterior septal accessory pathway and atrial flutter. An electrophysiological study after percutaneous balloon mitral valvotomy showed that the palpitations were due to atrial flutter with right bundle branch aberrancy. The right posterior septal pathway was a bystander because it had a higher refractory period than the atrioventricular node.
Percutaneous balloon dilatation, first described by
Andreas Gruentzig in 1979, was initially performed
without the use of guidewires.1 The prototype
balloon catheter was developed as a double lumen
catheter (one lumen for pressure monitoring or
distal perfusion, the other lumen for balloon inflation/deflation) with a short fixed and atraumatic
guidewire at the tip. Indeed, initially the technique
involved advancing a rather rigid balloon catheter
freely without much torque control into a coronary
artery. Bends, tortuosities, angulations, bifurcations,
and eccentric lesions could hardly, if at all, be negotiated, resulting in a rather frustrating low procedural success rate whenever the initial limited
indications (proximal, short, concentric, noncalcified) were negated.2 Luck was almost as
important as expertise, not only for the operator,
but also for the patient. It is to the merit of
Simpson who, in 1982, introduced the novelty of
advancing the balloon catheter over a removable
guidewire, which had first been advanced in the
target vessel.3 This major technical improvement
resulted overnight in a notable increase in the procedural success rate. Guidewires have since evolved
into very sophisticated devices.
Optical coherence tomography-guided algorithm for percutaneous coronary intervention. Vessel diameter should be assessed using the external elastic lamina (EEL)-EEL diameter at the reference segments, and rounded down to select interventional devices (balloons, stents). If the EEL cannot be identified, luminal measures are used and rounded up to 0.5 mm larger for selection of the devices. Optical coherence tomography (OCT)-guided optimisation strategies post stent implantation per EEL-based diameter measurement and per lumen-based diameter measurement are shown. For instance, if the distal EEL-EEL diameter measures 3.2 mm×3.1 mm (i.e., the mean EEL-based diameter is 3.15 mm), this number is rounded down to the next available stent size and post-dilation balloon to be used at the distal segment. Thus, a 3.0 mm stent and non-compliant balloon diameter is selected. If the proximal EEL cannot be visualised, the mean lumen diameter should be used for device sizing. For instance, if the mean proximal lumen diameter measures 3.4 mm, this number is rounded up to the next available balloon diameter (within up to 0.5 mm larger) for post-dilation. MLA: minimal lumen area; MSA: minimal stent area;NC: non-compliant
Brugada syndrome (BrS) is an inherited cardiac disorder,
characterised by a typical ECG pattern and an increased
risk of arrhythmias and sudden cardiac death (SCD).
BrS is a challenging entity, in regard to diagnosis as
well as arrhythmia risk prediction and management.
Nowadays, asymptomatic patients represent the majority
of newly diagnosed patients with BrS, and its incidence
is expected to rise due to (genetic) family screening.
Progress in our understanding of the genetic and
molecular pathophysiology is limited by the absence
of a true gold standard, with consensus on its clinical
definition changing over time. Nevertheless, novel
insights continue to arise from detailed and in-depth
studies, including the complex genetic and molecular
basis. This includes the increasingly recognised
relevance of an underlying structural substrate. Risk
stratification in patients with BrS remains challenging,
particularly in those who are asymptomatic, but recent
studies have demonstrated the potential usefulness
of risk scores to identify patients at high risk of
arrhythmia and SCD. Development and validation of
a model that incorporates clinical and genetic factors,
comorbidities, age and gender, and environmental
aspects may facilitate improved prediction of disease
expressivity and arrhythmia/SCD risk, and potentially
guide patient management and therapy. This review
provides an update of the diagnosis, pathophysiology
and management of BrS, and discusses its future
perspectives.
The Human Developmental Cell Atlas (HDCA) initiative, which is part of the Human Cell Atlas, aims to create a comprehensive reference map of cells during development. This will be critical to understanding normal organogenesis, the effect of mutations, environmental factors and infectious agents on human development, congenital and childhood disorders, and the cellular basis of ageing, cancer and regenerative medicine. Here we outline the HDCA initiative and the challenges of mapping and modelling human development using state-of-the-art technologies to create a reference atlas across gestation. Similar to the Human Genome Project, the HDCA will integrate the output from a growing community of scientists who are mapping human development into a unified atlas. We describe the early milestones that have been achieved and the use of human stem-cell-derived cultures, organoids and animal models to inform the HDCA, especially for prenatal tissues that are hard to acquire. Finally, we provide a roadmap towards a complete atlas of human development.
The treatment of patients with advanced acute heart failure is still challenging.
Intra-aortic balloon pump (IABP) has widely been used in the management of
patients with cardiogenic shock. However, according to international guidelines, its
routinary use in patients with cardiogenic shock is not recommended. This recommendation is derived from the results of the IABP-SHOCK II trial, which demonstrated
that IABP does not reduce all-cause mortality in patients with acute myocardial infarction and cardiogenic shock. The present position paper, released by the Italian
Association of Hospital Cardiologists, reviews the available data derived from clinical
studies. It also provides practical recommendations for the optimal use of IABP in
the treatment of cardiogenic shock and advanced acute heart failure.
Left ventricular false tendons (LVFTs) are fibromuscular
structures, connecting the left ventricular
free wall or papillary muscle and the ventricular
septum.
There is some discussion about safety issues during
intense exercise in athletes with LVFTs, as these
bands have been associated with ventricular arrhythmias
and abnormal cardiac remodelling. However,
presence of LVFTs appears to be much more common
than previously noted as imaging techniques
have improved and the association between LVFTs
and abnormal remodelling could very well be explained
by better visibility in a dilated left ventricular
lumen.
Although LVFTsmay result in electrocardiographic abnormalities
and could form a substrate for ventricular
arrhythmias, it should be considered as a normal
anatomic variant. Persons with LVFTs do not appear
to have increased risk for ventricular arrhythmias or
sudden cardiac death.
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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.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
2. Define
STEMI only
Urgent angioplasty(with/out
stenting)- Preferably in ≤90min
No TLT before or parallel
Open the infarct—related
3. Delayed PCI
PCI After TLT
1.Rescue(REACT/MERLIN/RESCU
E)
2.Facilitated(BRAVE/HERO/CAPI
TAL/WASTE/ASCEND)
Of its kinds
4.
5. STEMI
Thygesen K, Alpert JS, White HD, et al. Universal definition of myocardial
infarction. Circulation 2007;116:2634-53.
6. Today’s evening
• Abbreviating time is everything
1.Best transfer Protocol
2. Reverse Paradox
• PPCI vs. TLT
• Who need it?
• PPCI in Octagenerian
• Set up
1.Your Lab 2.Surgical Back up
7. Contd......
• Operator skill
• Initial therapy in ICCU
• Radial vs. Femoral
• Optimal anticoagulation
• POBA/ BMS/DES
• Hardware
• IABP/ECMO-When and its role
8. Contd....
• In cath lab
• After cathlab=ICCU
• Predischarge triage
• Finance
• Take home message
10. Time is muscle
Every minute counts
Gersh BJ, Stone GW, White HD, et al. Pharmacological facilitation of primary
percutaneous coronary intervention foracute myocardial infarction: is the slope of
the curve the shape of the future? JAMA 2005;293:979-86
11. Terkelsen CJ, Sorensen JT, Maeng M, et al. Systemdelay
and mortality among
patients with STEMI treated with primary percutaneous
coronary intervention.
JAMA2010;304:763-71.
12. Primary PCI vs. TLT
Choice
(TIMI)-3 Flow in 95% vs 54%(TLT)
Gersh BJ et al. Pharmacological facilitation of PPCI for STEMI: is
the slope of the curve the shape of the future? JAMA 2005;293:979-86
Stone GW et al. Comparison of angioplasty with stenting,with or without
abciximab, in acute myocardial infarction. N Engl J Med 2002;346:957-66
14. PAMI Trial-1997
POBA provides a small-to-moderate, short-term
clinical advantage over TLT with t-PA.
PPCI when it can be accomplished promptly at experienced
centers, should be considered an excellent alternative
method for myocardial reperfusion.
The investigators and centers participating in the GUSTO
IIb Angioplasty Substudy ,Cleveland Clinic,USA
15. A 2003 meta-analysis
23 randomized trials
7739 patients
Reductions in short-term death (7% vs 9%, P 0.0002),
fatal reinfarction (3% vs 7%, P 0.0001),
stroke (1% vs 2%, P 0.0004)
Keeley EC et al. Primary angioplasty versus intravenous thrombolytic
therapy foracute myocardial infarction: a quantitative review of 23
randomised trials. Lancet 2003;361:13-20
16. But TLT is the invaluable in certain conditions because delay in
opening artery causes
• CHF/ readmissions/OPD visits increases
independently with mortality(HR/OR=1.1)
detrimental in age<65, presenting within 2 hours
Death+ reinfarction+disabling stroke at 30
days was significantly < PCI in 2 of the
studies, with a trend toward significance in
the underpowered third study
31. Anticoagulants
‡The recommended ACT with planned GP IIb/IIIa receptor antagonist treatment is 200 to 250 s.
§The recommended ACT with no planned GP IIb/IIIa receptor antagonist treatment is 250 to 300 s (HemoTec device) or 300
to 350 s (Hemochron device).
34. Shock
• Killip IV
• Ionotrope optimum
• Control IV fluid
• CPR
• IABP/ECMO
• LVAD
• CABG
35. IABP but use it!!!!!!!!
• No Δ in infarct size at 3-5 days
• No Δ in all cause death at 6 months
Ohman EM, et al. Use of aortic counterpulsation to improve sustained coronary artery patency during AMI.RCT.
The Randomized IABP Study Group. Circulation 1994.
Stone GW et al, (PAMI-II) Trial Investigators. J Am Coll Cardiol 1997; 29:1459.
Brodie BR et al,IABP, before PPCI reduces catheterization laboratory events in high-risk patients with AMI . Am J
Cardiol 1999
Patel MR,et al. CRISP AMI Trial. JAMA 2011; 306:1329.
37. Manual aspiration thrombectomy
• 1.Microvascular function improves
• 2.Decrease death
• 3.MCE
I IIa IIb III
Cardiac death and reinfarction after 1 year in the Thrombus Aspiration during
Percutaneous coronary intervention in Acute myocardial infarction Study (TAPAS):
a 1-year follow-up study. Lancet. 2008;371:1915–20
Intracoronary abciximab and aspiration thrombectomy in patients with large
anterior myocardial infarction: the INFUSE-AMI randomized trial. JAMA. 2012;307:
1817–26
No reduction infarction size in large AWMI
39. Culprit vs. Bystanders
PCI should not be performed in a noninfarct artery at the time of
primary PCI in patients with STEMI who are hemodynamically
stable(2013 STEMI guideline).
I IIa IIb III
Preventive Angioplasty in Myocardial Infarction=PRAMI
2008 through 2013, at five centers in UK
465(234/234)
Subsequent PCI for inducible ischemia/refractory angina
composite of death/nonfatal MI/refractory angina
significantly reduced the risk of adverse cardiovascular events,
as compared with PCI limited to the infarct artery
40. STENTS
BMS/DES is useful
I IIa IIb III
BMS:High bleeding risk/noncomply with 1 year of DAPT/
anticipated invasive or surgical procedures in the coming year
I IIa IIb III
DES should not be used if unable to tolerate/comply with a
prolonged course of DAPT.
I IIa IIb III
Harm
41. POBA vs. BMS
tenting further reduced subsequent TLR but not
shown a survival advantage
1. Stone GW et al. Comparison of angioplasty with stenting,
with or without abciximab, in acute myocardial infarction. N Engl J Med
2002;346:957-66
2. Grines CL, Cox DA, Stone GW, et al. Coronary angioplasty with or without
stent
implantation for acute myocardial infarction. Stent primary angioplasty in
myocardial
infarction study group. N Engl J Med 1999;341:1949-56.
42. BMS vs. DES
DES greater reduction in TLR BUT not associated
with improved survival because added late ST
Stone GW et al. Paclitaxel-eluting stents versus bare-metal stents in acute
myocardial infarction. N Engl J Med 2009;360:1946-59.
Brar SS et al. Use of drug-eluting stents in acute myocardial infarction: a
systematic review and meta-analysis. J Am Coll Cardiol 2009;53:1677-89.
TYPHOON, PASSION, SESAMI, DEDICATION, and HORIZONS AMI
43. DES for STEMI
• TVR reduction >>BMS
• No extra stent thrombosis with DAP
• PCI with DES is not mandatory in STEM
• BMS may be preferable in cases in which comorbid
conditions, compliance, or financial means may
interfere with the required duration of dual-
antiplatelet therapy after DES placement
45. BMS Vs DES( G1)
• no significant difference in mortality, (8.5 versus 10.2
percent; HR 0.85,(95% CI 0.70-1.04).
• TLR was lower with DES (12.7 versus 20.1 percent; HR 0.57, 95% CI
0.50-0.66).
• No Δ in the cumulative rate of ST (5.8 versus 4.3 percent; HR 1.13, 95% CI
0.86-1.47). VLS (events after two years) was higher for DES (HR 2.81, 95%
CI 1.28-6.19).
• No Δ in the cumulative rate of reinfarction (9.4 versus 5.9 percent; HR
1.12, 95% CI 0.88-1.41). 2Y- the rate significantly increased for DES (HR
2.06, 95% CI 1.22-3.49).
De Luca G, et al. DES vs BMS in primary angioplasty: a pooled patient-level meta-a
46. BMS vs DES -G2
Cobalt-chromium everolimus-eluting stents (CoCr-EES)
• one-year risk of cardiac death/ MI was reduced with the former but not
the latter (odds ratio [OR] 0.63, 95% CI 0.42-0.92 and 0.86, 95% CI 0.50-
1.49).
• one-year risk TVR was reduced with the former but not the latter (OR 0.45,
95% CI 0.29-0.66 and 0.60, 95% CI 0.34-1.05).
• the one-year risk of definite stent thrombosis was reduced with the
former but not the latter (OR 0.32, 95% CI 0.11-0.78 and 0.44, 95% CI 0.12-
1.79).
• lower one-year rates of cardiac death or MI, definite stent thrombosis, and
target vessel revascularization
48. Drug-eluting balloon plus BMS
• First human trial
• not significantly different between the DEB-BMS
and BMS groups
• Drug is paclitaxel
Belkacemi A, J Am Coll Cardiol. 2012 Jun;59(25):2327-37. Epub 2012 Apr
11.
49. Direct Stenting
• significantly lower rate of all-cause death
• Lesser no flow/slow flow
• Better myocardial preservation
HORIZON AMI
Loubeyre C et al. A RCT of direct stenting with conventional stent implantation in selected patients with AMI . J Am Coll Cardiol
2002; 39:15.
Ly HQ et al. Angiographic and clinical outcomes associated with direct versus conventional stenting among patients treated with
fibrinolytic therapy for ST-elevation acute myocardial infarction. Am J Cardiol 2005; 95:383.
Antoniucci D, et al. Direct infarct artery stenting without predilation and no-reflow in patients with acute myocardial infarction.
Am Heart J 2001; 142:684.
50. Bioresorbable vascular Scaffolds
• Safe
• Feasible
• Available Size, short expiry is limitation
• Not approved/not guide lined
• Long term result awaited
PRAGUE-19 Study,87 pts/3 yrs//started in 2012/Abbott vascular
51. Intra coronary IIB-IIIA
inhibitor(abciximab)
Death+ reinfarction, p=0.03
Death ,p=0.04)
TVR ,p=0.045)
Reinfarction; p=0.13
Raffaele Piccolo et al,Italy,Meta analysis,2012, Heart doi:10.1136/heartjnl-
2011-301101
52. Intracoronary Adenosine
• A bolus injection of intracoronary adenosine (900
micrograms in 5 mL of 0.9% sodium chloride
solution). Control patients received an intravenous
bolus injection of adenosine (900 micrograms in 20
mL sodium chloride) during the procedure
• Elective intracoronary administration of high-dose
adenosine as adjunctive therapy to primary PCI
reduces MVO
53. INTRA CORONARY TLT
• 2.5 lakhs unit STK
• Improves no reflow
• Improves TFC
• EPICARDIAL coronary looks beautiful
• At 6 months ,no gain add to viable myocardium
Murat Sezer et al, Turkey, N Engl J Med 2007; 356:1823-1834,
57. Suboptimal reperfusion after
PPCI/Complication
Persistent stenosis or thrombosis
Coronary dissection
Intramural hematoma
Side branch occlusion
Coronary spasm
Distal macroembolism
Acute stent thrombosis
No-reflow phenomenon
Reperfusion injury
Capillary blistering and edema of endothelial cells
Edema and swelling of myocytes
PAMI:
Age ≥70 years
Diabetes
Longer time to reperfusion
Initial TIMI flow grade ≤1
Left ventricular ejection
fraction <50 percent
58. Ventricular Arrhythmias
• Immediate defibrillation or cardioversion for VF or
pulseless sustained VT,
• Early (within 24 hours of presentation)
administration of beta blockers.
• The prophylactic use of lidocaine is not
recommended.
• VPC, NSVT not associated with hemodynamic
compromise, and AIVR are not indicative of
increased SCD risk needs less attention.
59. No reflow phenomenon
• 10 – 30 %
• Influences the long term results of PCI significantly.
• Minimised by NTG(25 microgram). Verapamil,
diltiazem, GpIIBIIIA inhibitors, nikorandil(IONA),
thrombectomy, intracoronary STK, ischemic post
conditioning.
60. Rescue CABG < 3%
Aspirin should not be withheld
Short-acting intravenous GP IIb/IIIa receptor antagonists
(eptifibatide, tirofiban) should be discontinued at least 2 to 4
hours before urgent CABG.
Clopidogrel or ticagrelor should be discontinued at least 24 hours
before urgent on-pump CABG, if possible.
I IIa IIb III
I IIa IIb III
I IIa IIb III
61. RESCUE CABG
Abciximab should be discontinued at least 12 hours before
urgent CABG.
Urgent off-pump CABG within 24 hours of clopidogrel or
ticagrelor administration might be considered, especially if the
benefits of prompt revascularization outweigh the risks of
bleeding.
Urgent CABG within 5 days of clopidogrel or ticagrelor
administration or within 7 days of prasugrel administration
might be considered, especially if the benefits of prompt
revascularization outweigh the risks of bleeding.
I IIa IIb III
I IIa IIb III
I IIa IIb III
62. Role of third antiplatlet
Yes you may add,but
bleeding matters
63. Sheath removal timing
• ACT <160 SEC
• SHEATH SIZE α compression time
• USE OF Group IIA-IIIB inhibitors
• After 6 hrs for femoral and 2 hours for Radial
65. Very Elderly (≥85 Years)
Claessen et al. Primary percutaneous
coronary intervention for ST elevation
myocardial infarction in octogenarians: trends
and outcomes. Heart 2010;96:843–7
Danish Registry Supports
Primary PCI in Elderly STEMI
Patients-2013
Senior-PAMI-2005
66. Secondary prevention
• Beta Blockers: initiated in the first 24 hours
unless C/I
• Renin-Angiotensin-Aldosterone System
Inhibitors:within 24 hrs
• Lipid Management
67. Posthospitalization Plan of Care
•Prevent hospital readmissions
•Should be used to facilitate the transition to effective
•Outpatient care
I IIa IIb III
•Exercise-based cardiac rehabilitation
•Secondary prevention programs
I IIa IIb III
68. Posthospitalization Plan of Care
Medication adherence
Follow-up
Dietary and physical activities
Compliance with interventions for secondary prevention should
be provided to patients with STEMI.
No smoking
No secondhand smoke
I IIa IIb III
I IIa IIb III