amyloid .cardiac amyloidosis. Pathogenetic steps in the development of amyloid diseases.AL amyloidosis. ATTR amyloidosis.ATTRwt amyloidosis.
Potential for misdiagnosis of amyloidosis
amyloid .cardiac amyloidosis. Pathogenetic steps in the development of amyloid diseases.AL amyloidosis. ATTR amyloidosis.ATTRwt amyloidosis.
Potential for misdiagnosis of amyloidosis
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.
In this ppt i am going to discuss various spotters, including ECG, X-ray, fluroscopy images and there answers. These spotter now days asked in various DM cardiology exam conducted all over India, so it will help you in your DM Cardiology exam preperationn.
#flozins
🫀DAPA 🆚placebo in HFpEF
Now we have a positive trial!
⬇️18% in CV☠️ death or
worsening HF among LVEF>40%
⬇️ 21%heart failure
💥Results same for LVEF> 60% 🆚LVEF<60%
COMPARES OPTIMAL MEDICAL THERAPY WITH INVASIVE THERAPY IN A PATIENT WITH STABLE ISCHEMIC HEART DISEASE WITH MODERATE TO SEVERE MYOCARDIAL ISCHEMIA ON NON INVASIVE STRESS TESTING
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.
In this ppt i am going to discuss various spotters, including ECG, X-ray, fluroscopy images and there answers. These spotter now days asked in various DM cardiology exam conducted all over India, so it will help you in your DM Cardiology exam preperationn.
#flozins
🫀DAPA 🆚placebo in HFpEF
Now we have a positive trial!
⬇️18% in CV☠️ death or
worsening HF among LVEF>40%
⬇️ 21%heart failure
💥Results same for LVEF> 60% 🆚LVEF<60%
COMPARES OPTIMAL MEDICAL THERAPY WITH INVASIVE THERAPY IN A PATIENT WITH STABLE ISCHEMIC HEART DISEASE WITH MODERATE TO SEVERE MYOCARDIAL ISCHEMIA ON NON INVASIVE STRESS TESTING
At the bifurcation, the shear forces peak at the carina, creating areas of high endothelial shear stress.
The development of atherosclerosis in the LMCA has been linked to flow haemodynamics, with atherosclerotic plaques described at areas of low endothelial shear stress in the lateral wall of the bifurcation, opposite to the carina.
Conversely, the carina is often free from disease, probably owing to the protective effect of high shear stress against plaque formation.
The length of the LMCA also influences stenosis location and morphology. In short LMCA (<10 mm), lesions develop more frequently near the ostium than in the bifurcation (55% versus 38%), whereas in long arteries, lesions develop predominantly near the bifurcation (ostium 18% versus bifurcation 77%).
Furthermore, ostial lesions more frequently have negative remodelling, larger luminal areas, and less calcium than distal lesions.
In cardiology practice, we often come across patients presenting with anginal pain who undergo coronary angiogram which reveals either normal or non-obstructive epicardial coronaries. Importance is given to epicardial coronaries and the coronary microvasculature which could be the cause of angina is often overlooked. These patients are then labeled to have non-cardiac chest pain and musculoskeletal or psychogenic etiology is suggested. However, with growing interest in coronary microvasculature which are the tiny blood vessels at the tissue level in myocardium, diagnostic modalities and treatment options for coronary microvascular disease are being explored.
Arteriovenous Malformations are one of the toughest cerebral pathologies to manage with high post op mortality and morbidity. this powerpoint contains classification, grading and managment of various severity of AVMs
Stereotactic Radiosurgery of Arteriovenous Malformations Clinical White PaperBrainlab
Learn more: https://www.brainlab.com/radiosurgery-products/
Despite the low prevalence—between 0.04% and 0.52%—in the general population, intracranial arteriovenous malformations (AVMs) are the leading cause of nontraumatic intracerebral hemorrhage in people younger than 35 years old. Intracranial AVMs are congenital anomalies developing between the fourth and eighth week of intrauterine life. They consist of the persistence of connections between an artery and a vein without the interposition of a capillary bed, typically under a high-flow regimen.
Clinical Profile of Acute Coronary Syndrome among Young AdultsPremier Publishers
Acute Coronary Syndrome accounts for 30% of hospital admissions with cardiovascular diseases. The risk of this syndrome is increasing among the younger adults, and a deep insight into the clinical profile among these patients will help in devising a preventive strategy, in order to alleviate the morbidity and mortality due to the syndrome. A cross sectional study was done among 125 subjects admitted to our tertiary care hospital with Acute Coronary Syndrome. Their risk factors were assessed and a 12 Lead electrocardiogram and 2D Echocardiogram were taken. Cardio III panel which consists of Troponin I, CK MB, BNP by COBAS meter machine was also measured. STEMI was present in 73.6% of the patients, while unstable angina was present in 16%. About 90% of STEMI patients were males and 62% of them were hypertensives. LV Ejection Fraction <30% was found in 9% of STEMI patients. This study elucidates the need for a preventive strategy for primordial prevention of cardiovascular events among young adults. The study envisaged the male, urban preponderance towards these events.
Similar to MINOCA , Myocardial Infarction with Non-Obstructive Coronary Arteries (20)
Pro / Con Debate on Central Blood Pressuremagdy elmasry
The Basis : Forward & Reflected Pulse Waves
Central BP - Pro Side of the Argument
Central BP - Con Side of the Argument
Central BP - Consensus on Clinical Application
FDA-cleared devices for central BP and arterial stiffness assessment
Value of measuring central BP in clinComparative effect of
anti-hypertensive drugs and nitrates
on central systolic BP
ical practice
isolated systolic hypertension in the young
The cardio-metabolic continuum.
Hypertension and global cardio-metabolic risk
Hypertension Continuum Stages
What is the total cardiovascular risk?
What is the residual cardiovascular risk?
Global “Cardio-metabolic” Residual Risk Reduction
Residual CV risk rising from obesity.Metabolic syndrome.From NAFLD (Non-Alcoholic Fatty Liver Disease)
to MAFLD (Metabolic dysfunction-Associated Fatty Liver Disease)
Diagnosis and Management of Cardiovascular Involvement in Friedreich Ataxia
GAA 7-34 times→Normal
GAA 100-1700 times→FRDA
Current Research
into Drug Treatments
for Friedreich ataxia
Best Practice in Rare Diseases
Although CNS involvement dominates the clinical presentation of FRDA ,
CV involvement dictates its prognosis, accounting for ~ 59% of deaths among FRDA patients .
The prognosis is particularly poor for those with progressive LV systolic dysfunction.
Should we screen for and treat childhood dyslipidemia?
The Rationale for ASCVD Prevention by Primordial and Primary Strategies
Pediatric guidelines
Selective Screening
2Treatment algorithm of childhood dyslipidemia
-8 years & 12-16 years
Dyslipidemia and lipid lowering-therapy {LLT}
in women through the course of life. Lipid loering drug safety profile .Aging is associated with an increasing burden of morbidity, especially for CVDs.
Elderly population should be screened for
Main CV risk factors :
T2D , HTN , Smoking , Dyslipidemia & Obesity
Comorbidities : CKD
Geriatric conditions: Functional Impairment
Linking HFpEF and Chronic kidney disease magdy elmasry
Cardio-renal interactions
Introducing nephro-cardiology
{ or cardio-nephrology }
Where are we in 2022 with HFpEF ?CKD in HFpEF { or HFpEF in CKD } Cardiorenal
Syndrome .Four-step
HFA-PEFF diagnostic algorithm
heterogeneity in patients with HFpEF.Phenotyping HFpEF :
Beyond EF.Management of HFpEF .patients with HF on dialysis
Drug Treatment of Chronic Coronary Syndrome: Focus Issue on Ranolazinemagdy elmasry
Chronic Coronary Syndromes .Old and New Anti-anginal Drugs.Sodium channel blocker(Ranolazine)Angina / ischaemiac relief .
Voltage-gated sodium channels (NaVChs).Patient profile to guide drug treatment of
chronic coronary syndromes .Therapeutic algorithm for chronic stable angina according to heart rate and blood pressure.Treatment Options for Microvascular angina / Vasospastic angina.Ranolazine in arrhythmias
Ranolazine in ischemic reperfusion injury
Ranolazine in pulmonary hypertension
Ranolazine in heart failure
Ranolazine in the prevention of chemotherapy‑induced cardiotoxicity
Role in diabetes mellitus
Ranolazine in peripheral arterial disease
Ranolazine in myotonia‑congenita
Ranolazine in hypertrophic cardiomyopathy.Antiarrhythmic properties of ranolazine.Amiodarone +Ranolazine
Strategies to improve adherence to antihypertensive medicationmagdy elmasry
Challenges in hypertension treatment.What is the definition of medication non-adherence?Who is at risk? How should
patients at risk be screened and identified?What are the negative impacts of non-adherence?What is the
practical approach for improving adherence? The ABC taxonomy for medication adherence
Adherence :3 quantifiable components: initiation , implementation , and discontinuationThe five dimensions
of non-adherence
.
Do T2DM drugs have CV benefit for Type 1 Diabetes ?magdy elmasry
T1D Exchange , average A1C levels have not improved .How can adjunctive therapies ( added to insulin ) can help?
The Removal Trial.Three main clinical trials :
DEPICT with dapagliflozin ,
EASE with empagliflozin , and
inTANDEM with sotagliflozin.
Takotsubo syndrome diagnostic criteria.
position papers :Mayo clnic ,HFA and InterTAK Diagnostic Criteria.Takotsubo Syndrome and COVID-19.Noninvasive Multimodality Imaging
in the Diagnosis and Management
of Patients with Takotsubo Syndrome
CVD in cancer survivors.Screening of cancer survivors.Chest Radiotherapy .JACC Scientific Expert Panel
( J Am Coll Cardiol 2019;74:905–27 )manifestations of chest and mediastinal radiotherapy .
Connections Between Hepatic and Cardiovascular Disease,Diagnostic criteria for cirrhotic cardiomyopathy 2005 and 2019.New CCM criteria based
on contemporary CV imaging parameters
LV Systolic Function.
LV Diastolic Dysfunction.cardiac evaluation algorithm for liver transplant candidates
Anti-Diabetics For Cardiac Patients The Proper Selectionmagdy elmasry
Cardiovascular Disease and Type 2 Diabetes.Tight glycaemic control can reduce microvascular complications of T2DM, but does not lower CV risk sufficiently.
Multifactorial intervention, comprising of lowering lipid levels and BP, and use of aspirin, has been shown to reduce vascular complications and mortality.Shifting the Paradigm in Diabetes Care
Treating Diabetes Beyond A1C :Considerations for Cardiovascular Protection.
Peripartum Cardiomyopathy .BOARD scheme for the therapy of patients with acut...magdy elmasry
Definition of peripartum cardiomyopathy;Risk factors for the development of PPCM .Environmental Factors
Vasculohormonal (pregnancy).Genetic Factors Titin-truncating
Variants (TTNtv) .Secretion of prolactin by the anterior pituitary gland, upregulation of endothelial microRNA-146a (miRNA-146a), and placental secretion of soluble fms-like tyrosine kinase receptor 1 (sFlt-1) lead to endothelial dysfunction and cardiomyocyte death.Antisense therapy against microRNA-146a
Prolactin inhibition.bromocriptine .biomarkers in peripartum cardiomyopathy
Thyroid Hormones and Cardiovascular Function and Diseasesmagdy elmasry
Thyroid hormone system.
Thyroid hormone action on the CVS.
Thyroid hormones and cardioprotection.
How does thyroid disease affect the heart?
- Thyroid disease and CV risk factors.
- Thyroid dysfunction and CVD.
Thyroid hormones : a future therapeutic option?
New recommendations for a thyroid and CVD.
Thyroid and CV drugs.
Chronic Obstructive Pulmonary Disease and Heart Failure The challenges facin...magdy elmasry
Chronic Obstructive Pulmonary Disease and Heart Failure
The challenges facing cardiologists and pulmonologists,
prevalence of heart failure in COPD patients .Association of Cardiovascular Disease With Respiratory Disease,An atypical presentation of myocardial infarction (MI) should be considered in every patient presenting with COPD exacerbation ,Cardiovascular and pulmonary disease in the context of inflammation
(“CardioPulmonary Continuum”),The cornerstones of therapy are beta-blockers and beta-agonists ,which as their modes of action suggest oppose each other’s action
The main hemodynamic interactions that may impact on the diagnosis of multiple and mixed Multiple and Mixed Valvular Heart Diseases:HOW TO USE IMAGINGThe interplay of multiple valve pathology.The clinical challenge of concomitant aortic and mitral valve stenosis
.
.
Cancer-Associated Thrombosis.From LMWH to DOACsmagdy elmasry
Cancer-Associated Thrombosis.Risk factors for CAT. Certain types of cancer are associated with higher risk of CAT. Anticoagulant therapy for VTE in patients with cancer
Should You Use DOACs for Cancer-Associated VTE?.Criteria for DOAC use in cancer patients requiring anticoagulation .DOACs + AntiCancer agents
The Progression of Hypertensive Heart Disease.From hypertension to heart failuremagdy elmasry
Staging of Hypertensive Heart Disease.Precipitants and clinical sequelae related to LVH and myocardial fibrosis.Imaging in hypertensive heart disease .Differential diagnosis of LVH.Concentric LVH .Eccentric LVH . Concentric remodeling .linking hypertension and atrial fibrillation
Role of the Renin–Angiotensin–Aldosterone System Inhibition Beyond BP Reductionmagdy elmasry
Hypertension Mediated Organ Damage : How We Prevent It?The Role Of RAAS In Cardiovascular Continuum.Changes in Arterial Diameter in Patients with Arteriosclerosis or Atherosclerosis.Not All Angiotensin-Converting Enzyme Inhibitors Are Equal.Question : ACEIs vs. ARBsIs One Class Better For Cardiovascular Diseases?BP Variability .Central BP
.
Vascular Age &
Arterial Stiffness.Achieving BP Goals.
Cardio-Renal Protection Through Renin–Angiotensin–Aldosterone System Inhibitionmagdy elmasry
Physiological and detrimental roles of RAAS molecules in cardiac, vascular tissues and kidneys.‘cardiovascular continuum’ Barriers In Optimizing RAAS Inhibition.The effects of angiotensin II inhibition and improvement in bradykinin availability
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
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
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
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
2. A Changing Philosophy
Nonobstructive disease is not a false positive. It's not benign.
Non-obstructive Coronary Arteries
Myocardial InfarctionIschemia
3. Normal coronary angiogram. A smooth patent covetable left main, LAD, and circumflex
projected from the screen. Next to these innocent-appearing vessels was a distinctly sinister
IVUS study from the same angiogram demonstrating plaque rupture and ulceration.
The finding of angiographically
smooth coronary arteries does
not preclude an aetiologic role of
thrombotic disease in MINOCA.
4. What we can see is only 5% of the total coronary tree.
? Coronary
Microvascular Dysfunction
Non-obstructive Coronary Arteries
5. Mechanisms for ischemic heart disease in women.
*Plaque disruption denotes plaque rupture or plaque erosion
7. A potential problem with current AMI criteria is their
central focus upon troponins, since clinicians encounter
elevated troponins in clinical scenarios other than AMI.
10. MINOCA should be considered as a ‘working diagnosis’,
analogous to heart failure, and thus prompts further
evaluation regarding its underlying mechanism(s).
11.
12. MINOCA:
A case study of a 55-year-old woman with an anterior STEMI presentation.
20. CMR imaging is a key investigation
in identifying the underlying cause
21. Coronary angiography portraying subtle
lesion (arrow) involving the mid LAD
Cardiac MRI revealing LGE of the mid to distal
anteroseptal wall (arrows).
Still frames from horizontal long axis (top
row) and short axis (bottom row) are
consistent with mid to distal LAD infarction
Ann Clin Lab Res. 2016, 4: 3.
22. Bar graph of published studies showing the diagnostic significance
of CMR imaging in MINOCA patients.
Data presented as percentage (%).
Cardiac magnetic resonance (CMR) imaging findings in patients with MINOCA.
23. Management
A fundamental consideration is
identifying the underlying cause of
this heterogeneous syndrome
because that will determine
appropriate therapy.
24. All-Cause Mortality in Patients With MINOCA or MI-CAD
Data presented as percentage (%) and 95% confidence intervals (%) with
odds ratio (OR) and P values.
MI-CAD indicates myocardial infarction with coronary artery disease; and
MINOCA, myocardial infarction with nonobstructive coronary arteries
Circulation 2015;131(10):861–870
MINOCA : is not a benign condition?
25. Guarded Prognosis
Hence patients with MINOCA should receive the
same clinical attention as AMI patients who have
single- or double-vessel disease and not merely
dismissed as having an insignificant clinical
condition.
Although the outcome of MINOCA strongly
depends on the underlying cause, its overall
prognosis is serious, with a 1 year mortality of
about 3.5%.
32. Dr. Noel Bairey Merz is the director of the Barbra Streisand Women's Heart Center at Cedars Sinai and is a leader in female
cardiovascular treatment. "In a session on New Practice Patterns in Clinical Cardiology at the European Society of Cardiology 2017
Congress, she gave a presentation titled "A Women's Clinic for Heart Disease." Her talk outlined three distinct sub clinic options
where women with heart disease can seek help: The MINOCA (myocardial infarction without obstructive coronary artery disease)
clinic, the HFpEF (heart failure with preserved ejection fraction) clinic, and the APO (adverse pregnancy outcomes) clinic."
We have an
evidence gap,
“she concluded”
MINOCA
research
needed !