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
New ESC guideline on cardiovascular disease in pregnancyArunSharma10
New ESC Guideline on Cardiovascular Disease in Pregnancy
Management of Cardiovascular Diseases During Pregnancy
Women with CVD
LMWH
Drugs during pregnancy and breastfeeding
Valvular heart disease
Coronary artery disease
Pregnancy is complicated by maternal disease in 1–4% of cases
EMGuideWire's Radiology Reading Room: Peripartum CardiomyopathySean M. Fox
The Department of Emergency Medicine at Carolinas Medical Center is passionate about education! Dr. Michael Gibbs is a world-renowned clinician and educator and has helped guide numerous young clinicians on the long path of Mastery of Emergency Medical Care. With his oversight, the EMGuideWire team aim to help augment our understanding of emergent imaging. You can follow along with the EMGuideWire.com team as they post these educational, self-guided radiology slides or you can also use this section to learn more in-depth about specific conditions and diseases. This Radiology Reading Room pertains to Peripartum Cardiomyopathy and is brought to you by Kaley El-Arab, MD, Blaire Langa, NP, Claire Lawson, NP, and Ashley Moore Gibbs, DNP. It is has the special guest editors: Richard Musialowski, MD and Laszlo Littmann, MD.
New ESC guideline on cardiovascular disease in pregnancyArunSharma10
New ESC Guideline on Cardiovascular Disease in Pregnancy
Management of Cardiovascular Diseases During Pregnancy
Women with CVD
LMWH
Drugs during pregnancy and breastfeeding
Valvular heart disease
Coronary artery disease
Pregnancy is complicated by maternal disease in 1–4% of cases
EMGuideWire's Radiology Reading Room: Peripartum CardiomyopathySean M. Fox
The Department of Emergency Medicine at Carolinas Medical Center is passionate about education! Dr. Michael Gibbs is a world-renowned clinician and educator and has helped guide numerous young clinicians on the long path of Mastery of Emergency Medical Care. With his oversight, the EMGuideWire team aim to help augment our understanding of emergent imaging. You can follow along with the EMGuideWire.com team as they post these educational, self-guided radiology slides or you can also use this section to learn more in-depth about specific conditions and diseases. This Radiology Reading Room pertains to Peripartum Cardiomyopathy and is brought to you by Kaley El-Arab, MD, Blaire Langa, NP, Claire Lawson, NP, and Ashley Moore Gibbs, DNP. It is has the special guest editors: Richard Musialowski, MD and Laszlo Littmann, MD.
Peripartum cardiomyopathy (PPCM) is a type of heart disease that affects women during the last month of pregnancy or in the first few months after delivery. It is characterized by a weakened and enlarged heart muscle, which makes it difficult for the heart to pump blood efficiently to the rest of the body. The exact cause of PPCM is unknown, but it is believed to be related to the hormonal changes and increased demands on the heart that occur during pregnancy. Symptoms of PPCM can include shortness of breath, fatigue, chest pain, swelling in the legs and feet, and palpitations. Treatment for PPCM usually involves medications to improve heart function and supportive care to manage symptoms. In severe cases, advanced treatments such as implantable devices or heart transplantation may be necessary. With early diagnosis and treatment, most women with PPCM can recover completely and go on to lead healthy lives.during pregnancy.
The diagnosis of PPCM is based on clinical symptoms, such as shortness of breath, fatigue, chest pain, and edema, along with imaging studies, such as echocardiography. Treatment for PPCM usually involves medications to improve heart function and supportive care to manage symptoms. These medications can include beta-blockers, ACE inhibitors, diuretics, and inotropic agents. In severe cases, advanced treatments such as mechanical circulatory support or heart transplantation may be necessary.
The prognosis for PPCM varies depending on the severity of the disease and the presence of underlying comorbidities. However, with early diagnosis and appropriate treatment, most women with PPCM can recover completely and go on to lead healthy lives. The recurrence rate of PPCM in subsequent pregnancies is approximately 20%, and women who have had PPCM are advised to avoid future pregnancies or undergo careful monitoring and management during pregnancy.
There are still many unanswered questions about PPCM, including its exact cause, optimal diagnostic and treatment strategies, and long-term outcomes. Further research is needed to better understand this complex and potentially life-threatening condition.
In conclusion, PPCM is a rare but serious form of heart disease that can occur during or after pregnancy. Early recognition and management of this condition are critical in preventing complications and improving outcomes for both the mother and the baby. Future research will continue to shed light on the pathophysiology and optimal management of PPCM.
Peripartum cardiomyopathy (PPCM) is a rare form of heart failure that occurs during the last month of pregnancy or within the first five months postpartum. It presents significant challenges in diagnosis and treatment due to its overlap with symptoms of normal pregnancy and postpartum changes. This condition varies in incidence across different racial groups and geographical locations, with a notable occurrence in the United States and southern India.
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.
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
HDL-cholesterol concentrations are inversely associated with CVD.When we consider cardiovascular mortality in women in terms of HDL.Causes of low HDL cholesterol.Lipoprotein subfractions suffer a shift after menopause towards a more atherogenic lipid profile.associations of HDL-C and HDL-P with cIMT and CHD.MESA (Multi-Ethnic Study of therosclerosis. Functional Versus Dysfunctional HDL. High concentrations of HDL - cholesterol are associated with high all-cause mortality in men and women.Improvement of HDL function without necessarily raising HDL-C
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 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
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.
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
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
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.
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
2. Today’s talk will include:
Historical Context
Definition
Epidemiology
Risk Factors
Patho-physiology & Novel Therapies
Clinical Presentation & Differential Diagnosis
Diagnostic Workup
Treatment & Breast feeding
Prognosis
Counseling / Subsequent Pregnancy
Contraception
Knowledge Gap
How to see the big picture is not as easy as you'd think.
4. The first description of idiopathic myocardial failure with onset in the
puerperium has been attributed to Ritchie in 1849.
Ritchie C. Edinb Med Surg J. 1849;2:333–342.
Clinical contribution to the pathology, diagnosis, and treatment of
certain chronic diseases of the heart.
5. The 19th
(nineteenth)
century
The 20th
(twentieth)
century
The 21st
(twenty first)
century
Ritchie C
(1849)
Gouley BA et al
(1937)
&
Hull E and
Hafkesbring E
(1937)
There is a crisis in
academic publishing (Too
much academic research
is being published)
PPCM
9. Definition of peripartum cardiomyopathy
1. Heart failure secondary to left ventricular
systolic dysfunction with a LVEF < 45%
2. Occurrence towards the end of pregnancy or in
the months following delivery (mostly in the month
following delivery)
3. No other identifiable cause of heart failure
Diagnosis is often always by exclusion
11. Worldwide variation in incidence of PPCM
Incidence seems to be highest in
Nigeria (one in 100 live births) and Haiti (one in 300 live births)
Haiti Nigeria
12. *The unit of population differs among studies depending on the population representing all births, live births (excluding stillbirth), deliveries,
hospitalizations, and women. †Although there are several reports from the United States, the report by Kolte, et al was selected because it
includes the most recent data.(Isogai, et al. Int Heart J May 2019)
Maternal mortality rate and incidence of PPCM in various countries
Significant Geographical Variations
The incidence of PPCM and the maternal mortality rate were well correlated
13. CONCLUSION
Yes, we can prevent peripartum cardiomyopathy, but
such a challenge involves changing the way of life of millions
of people and effectively fighting poverty.
SL Clinical and Experimental Cardiology. 2019; 2(1):117
Yes, we can prevent peripartum cardiomyopathy, but…
15. Risk Factors for the Development of PPCM
Risk factors for the development of PPCM have been classified as probable (twin pregnancy, high parity/gravidity,
extreme reproductive age and prolonged tocolysis);proposed (smoking, hypertension, malnutrition, cocaine use,
African ancestry and socioeconomic status); and emerging (genetics, pre-eclampsia and obesity).
17. Etio-pathogenesis (etiology and pathophysiology ) of PPCM : ???
Hemodynamic stress
Viral myocarditis—coxsackievirus, echovirus, parvovirus B19
Microchimerism—myocyte engraftment with immune dysfunction
Genetic factors—mutations of cardiac genes—TTNC1, TTN, STAT3
Antiangiogenic factors—sFlt-1 inhibition of VEGF
Prolactin—increased cathepsin D peptidase
Possible Causes or Triggering Events for PPCM
Proposed
pathogenesis :
a “two-hit
hypothesis.”
Environmental
Factors
Vasculohormonal
(pregnancy)
Genetic
Factors
Titin-truncating
Variants (TTNtv)Affected
PPCM is likely caused by a complex interaction of
genetic and environmental factors
18. The Pathophsiology of PPCM is uncertain.
Current thinking favors a “two hit” model of PPCM pathogenesis
How do vasculo-hormonal insults interact with underlying genetic susceptibility
to produce PPCM ?
First hit
Genetic predisposition
Gene mutations : e.g. TTN gene
Second hit
Antivascular or hormonal effects
↑Prolactin (PRL)→16-kDa (vasoinhibin)
↑Soluble fms-like tyrosine kinase receptor 1
(sFlt-1):Angiogenic Imbalance
Pituitary
Placenta
19. Representative diagram of titin’s position in myocyte architecture.
Titin extends from the Z-disk of the sarcomere (N-terminus) to the M-band (C-terminus).
The central part of the protein contains I-band region (I) and A-band region (A).
Titin-truncating mutations :
Titin-truncating variants (TTNtv)→Sarcomere insufficiency →DCM /PPCM
20. 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
Pathophsiology of PPCM : a vascular/hormonal hypothesis
sFlt-1
inhibition of VEGF
(Antiangiogenic)
(PRL fragment:
vasoinhibin)
a
21. One of the new strategies for treating PPCM is based on this knowledge :
Prolactin inhibition.
Blocking PRL completely by use of bromocriptine eliminates
pathophysiological 16K PRL, but also nursing ability.
Class IIb
Recommendation
22. Emerging treatments :
Antisense therapy against microRNA-146a
Use of anti-miR-146a in less severely affected patients may
improve PPCM recovery, while keeping normal nursing functions.
Note: MicroRNA-146a is a therapeutic target and biomarker for PPCM
? Investigational
24. PPCM : a diagnostic challenge
Since no specific test to confirm PPCM exists,
it remains a diagnosis of exclusion, and differential diagnoses
need to be considered.
25. Is it PPCM or normal pregnancy ?
Shortness of breath
Fatigue
Leg swelling
Tachycardia
The major symptoms of PPCM are those of heart failure and include fatigue, shortness of
breath, tachycardia ,and fluid retention.
Because there is a significant overlap between symptoms related to pregnancy, especially
toward the end of the third trimester or after delivery, and heart failure , the diagnosis
may be initially missed or delayed.
27. Is it PPCM or Preeclampsia ?
Pre‐existing or new‐onset
hypertension, proteinuria
During second trimester of pregnancy
LVH, diastolic dysfunction
No known cardiac disease, no HF signs
and/or symptoms prior pregnancy
Towards the end of pregnancy and the
months following delivery
LVEF < 45%
Overlapping Diseases of Pregnancy
33. Pragmatic evaluation scheme for suspected acute PPCM during the end of pregnancy or the
months after delivery. Measurement of natriuretic peptides and echo are recommended to
quickly strengthen or rule out the diagnosis of PPCM.
Symptoms during end of pregnancy or
months following delivery: dyspnoea,
orthopnoea, peripheral oedema, chest
pain, dizziness, palpitations, fatigue,
depression, cough
35. PPCM : a therapeutic challenge
To consider both the health of the mother and the foetus or baby
36. It is important to exclude drugs that may have a harmful effect on the
developing foetus or those that are contraindicated during breastfeeding
[ACEI, ARB , ARNI, k-sparing diuretics, warfarin, and ivabradine]
Acute heart
failure/cardiogenc shock
Stabilized/chronic heart
failure
According to the latest guidelines of the ESC 2018, the treatment of PPCM does
not deviate from the recommendations used in acute HF, cardiogenic shock, or
chronic HF of a different aetiology.
37. Safety of drugs for PPCM during pregnancy and lactation
Drug Use during pregnancy Potential adverse effects Use during lactation†
Loop diuretics
Compatible (most experience with
furosemide)
Maternal hypovolemia and
hypotension, resulting in
uterine hypoperfusion
Compatible
(overdiuresis may
decrease breast milk
production)
β blockers Compatible
Fetal bradycardia, fetal
hypoglycemia
Compatible
ACE inhibitors and ARBs Incompatible
Renal agenesis,
oligohydramnios,
malformations, fetal demise
Compatible (captopril,
enalapril, quinapril,
benazepril)
Mineralocorticoid receptor
antagonists
Incompatible Undervirilization of the fetus Compatible
Sacubitril-valsartan Incompatible
Same as ACE
inhibitors/ARBs
Unknown (lack of
data)
Hydralazine/nitrates Compatible
Maternal hypotension,
resulting in uterine
hypoperfusion
Compatible
Ivabradine
Not recommended (worrying results in
animal studies, no studies in humans)
Unknown
Unknown (lack of
data)
Digoxin Compatible Low birth weight Compatible
Heparin (unfractionated and
low molecular weight)
Compatible Does not cross placenta Compatible
Warfarin
Avoid if possible owing to
teratogenicity
Warfarin embryopathy
(skeletal deformities),
intracranial hemorrhage,
spontaneous abortion,
stillbirth
Compatible
Direct-acting oral
anticoagulants (eg,
rivaroxaban, apixaban,
edoxaban, dabigatran)
Incompatible
Limited data suggest
possible malformations,
growth restriction
Currently discouraged
owing to lack of data
38. Subacute HF
Hemodynamic stability
Acute HF
Hemodynamic stability
Respiratory insufficiency
Cardiogenic shock
Hemodynamic instability
Respiratory insufficiency
Mild PPCM
Moderate PPCM
Severe PPCM
Normal ward, ambulatory
treatment in selected patients
possible
Intermediate care (IMC), HF unit
(HFU)
Intensive care unit (ICU)
Oral HF drugs
Oral diuretics in case
of fluid overload
Consider
bromocriptine for 1
week
– Diuretics i.v.
– Consider vasorelaxants if SBP
>110 mmHg
– Supplemental O2 , non-invasive
ventilation if necessary
– Avoid inotropes/catecholamines
– Consider bromocriptine for 8
weeks if LVEF <25%
- Oral HF drugs
– Diuretics i.v.
– Inotropes/catecholamines if
needed
– Invasive ventilation
– Mechanical circulatory support
(Impella and/or ECMO)
– Consider bromocriptine for 8
weeks , uptitration depending on
prolactin levels
– Oral HF drugs after stabilization
Overview of different clinical scenarios in patients with PPCM.
39. The wearable
cardioverter-defibrillator (WCD)
The implantable
cardioverter defibrillator (ICD)
Because LV recovery is common in PPCM, the decision to insert an ICD
in a patient who initially presents with an LVEF <35% could be delayed,
and a WCD could be considered instead.
The WCD could be used as ‘bridging therapy’ until the LVEF is re-evaluated at follow up.
ICDs are best reserved for patients with PPCM without LV recovery after 6 months.
LVEF <35%
40. If a patient cannot be
stabilised
haemodynamically,
urgent delivery by
caesarean section is
necessary.
Vaginal delivery is preferred in
haemodynamically stable
patients.
Delivery
41. Breastfeeding : Breastfeeding in patients with PPCM is controversial
JACC 2019
LevelClassRecommendations
BIIbDue to the high metabolic demands of lactation and
breastfeeding, preventing lactation may be considered in
patients with severe HF
BIIbIn patients with PPCM, bromocriptine treatment may be
considered to stop lactation and enhance recovery (LV function).
CIIaBromocriptine treatment should be accompanied by prophylactic
(or therapeutic) anticoagulation
2018 ESC Guidelines for the management of CVDs during pregnancy
42. The treatment of PPCM, should consists of Bromocriptine, Oral heart failure therapies, Anticoagulation, vasoRelaxing
agents, and Diuretics. Non-invasive ventilation should be added in patients with pulmonary congestion.
BOARD scheme for the therapy of patients with acute PPCM.
Of note, this scheme addresses patients after delivery who do not breastfeed.
43. ICU = intensive care unit; LVEF = left ventricular ejection fraction; MCS, mechanical circulatory support (e.g. extracorporeal membrane
oxygenation, percutaneous microaxial pump); RV = right ventricle.
Scheme for Bromocriptine Treatment of Acute PPCM
Cardiac Failure Review 2018;4(1):46–9
If bromocriptine treatment is considered (class IIb recommendation),
different regimens are recommended according to disease severity.
45. Up to 72% of women with PPCM have
improvement in LVEF ,
but increased LV remodeling (LVEDD ≥6.0 cm)
, black race , and initial LVEF
< 30 % are poor prognostic factors
72% achieved an
LVEF ≥ 50 %
(J Am Coll Cardiol 2015;66:905–14)
Poor Predictors of outcome ( poorer recovery )
Race : black women
LV dysfunction (LVEF) : < 30%
LV remodeling (LVEDD): ≥6.0 cm
46. Worse NYHA functional class
LVEF ≤ 25%
Black race
Multiparity
Age more than 35 years
Risk factors
for increased
mortality in PPCM
"Rest In
Peace"
Maternal mortality
The mortality rate varies
from <2% to 50%.
52. It should be remembered that the right form of
contraception is the key to prevent the recurrence of PPCM.
What is the right birth control for me?
53. 1 A condition for which there is no restriction to use
2 A condition for which the advantages of use outweigh the theoretical or proven risks
3 A condition for which the theoretical or proven risks outweigh the advantages
4 A condition for which the method should not be used
The 2016 CDC-MEC (Centers for Disease Control and Prevention Medical Eligibility Criteria)
Simplified schema for contraceptive choices in PPCM and DCM
Current Heart Failure Reports (2018) 15:161–170
CHC = combined hormonal
contraceptive
PC = progestin-only
contraceptive
IUD = intrauterine
device
EC = emergency
contraception
55. "Research Gap" or "Knowledge Gap"
Knowledge gaps in PPCM research :
Pathogenesis
Diagnosis
Management
56. Another key unanswered question about the management of
PPCM is the optimal treatment of women with recovered LVEF,
who make up the majority of cases.
Length of treatment for patients with PPCM with recovered LVEF
Treatment is recommended for at least 12 months after recovery
of both the left ventricular EF and dimensions.
A period of time without medication and with recurrent
echocardiograms is ideal for confirming that the EF does not
deteriorate before a decision regarding a new pregnancy
HF reduced EF HF recovered EF
57. What do you do when doctors fail to properly treat or
misdiagnose PPCM ? See you in court
PPCM-related malpractice lawsuits
Editor's Notes
Proposed pathogenesis of peripartum cardiomyopathy: 1) genetic predisposition caused by mutations of various genes (STAT3, TTN, TTNC1) that regulate cardiomyocyte function causes secretion of cathepsin D (CathD), which cleaves pituitary prolactin (PRL) to form a 16-kDa fragment, vasoinhibin; 2) vasoinhibin acts on blood vessels to trigger apoptosis as well as microRNA-146α resulting in cardiomyocyte ischemia, metabolic insufficiency, and apoptosis. Simultaneously, the placenta, especially with the preeclampsia syndrome, secretes soluble fms-like tyrosine kinase 1 (sFlt-1), which neutralizes vascular endothelial growth factors A and B (VEGFA and VEGFB, respectively) that are critical for vascular health. MnSOD, mitochondrial antioxidant manganese superoxide dismutase; ROS, reactive oxygen species. Data from Arany Z, Elkayam U. Peripartum cardiomyopathy. Circulation 2016;133:1397–409; and Arany Z. Understanding peripartum cardiomyopathy
In heart (cardiac) muscle contraction, a main player is the protein titin (molecular mass of up to ~3800 kDa), encoded by the TTN gene (chromosome 2q31.2, ID: 7273, 363 exons). Titin extends from the Z-disk of the sarcomere (N-terminus) to the M-band (C-terminus) of the half sarcomere. The central part of the protein contains an elastic I-band region and a thick filament-binding A-band region
Biomarkers can help distinguish PPCM from other related pregnancy symptoms. N-terminal pro–B-type natriuretic peptide (NT-proBNP) has been shown to be elevated in PPCM. Other biomarkers that have been associated with PPCM include: 16-kDa prolactin, interferon-y, asymmetric dimethylarginine (ADMA), cathepsin D, soluble fms-like tyrosine kinase-1 (sFlt-1), and microRNA-146a.
MicroRNA-146a has been shown to be specifically increased in the serum of PPCM patients.