Hypertrophic cardiomyopathy
European society of cardiology guidelines,2014
Prevention of sudden cardiac death
Left ventricular outflow tract obstruction
http://www.theheart.org/web_slides/1416535.do
A trial to compare Fractional Flow Reserve versus Angiography for Guiding PCI in Patients with Multivessel Coronary Artery Disease II
http://www.theheart.org/web_slides/1416535.do
A trial to compare Fractional Flow Reserve versus Angiography for Guiding PCI in Patients with Multivessel Coronary Artery Disease II
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
This is a comprehensive description of coronay lesion assessment from routinely used angiography to advanced imaging modalities like IVUS/OCT including their functional significance by FFR
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
Use of adjunct devices like cutting balloon, rotaablation, excimer laser,mechanical thrombectomy and EPD in complex PCI improve procedural success and reduce restenosis rate.
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
This is a comprehensive description of coronay lesion assessment from routinely used angiography to advanced imaging modalities like IVUS/OCT including their functional significance by FFR
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
Use of adjunct devices like cutting balloon, rotaablation, excimer laser,mechanical thrombectomy and EPD in complex PCI improve procedural success and reduce restenosis rate.
Here\'s my project for school which we\'ll present next week I believe (week of Jan. 11). Dr. Quinn and/or Terry, it would be great if you could comment, that way I can say it has been reviewed by some medical authorities. :D Thanx!
Alcohol septal ablation is emerging as an alternative to surgical myectomy in the management of symptomatic cases of Hypertrophic obstructive cardiomyopathy (HOCM). This involves injection of absolute alcohol into 1st septal perforator thereby producing myocardial necrosis with resultant septal remodelling within 3-6 months. This results in reduction of septal thickness and LV outflow gradients with improvement in symptoms.
Early and effective treatment of patients with acute coronary syndrome saves lives. Lot of progress has been made in last few years in understanding patho-physiology and management of these patients.
Austin Spine is an open access, peer reviewed, scholarly journal dedicated to publish articles covering all areas of Spine.
The journal aims to promote latest information and provide a forum for doctors, researchers, physicians, and healthcare professionals to find most recent advances in the areas of Spine. Austin Spine accepts research articles, reviews, mini reviews, case reports and rapid communication covering all aspects of Spine.
Austin Spine strongly supports the scientific up gradation and fortification in related scientific research community by enhancing access to peer reviewed scientific literary works. Austin Publishing Group also brings universally peer reviewed journals under one roof thereby promoting knowledge sharing.
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
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
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.
4. The guideline is fairly long and detailed
(55 pages, with 506 references, and
36 tables listing recommendations).
0Data derived from multiple randomized
clinical trials or meta-analyses.
Level of
Evidence A
36
(27%)
Data derived from a single randomized
clinical trial or large non-randomized studies.
Level of
Evidence B
96
(73%)
Consensus of opinion of the experts and/ or
small studies, retrospective studies, registries.
Level of
Evidence C
132 recommendations in the guideline
5. 1) Etiologic diagnosis.
2) Diagnostic criteria.
3) Diagnostic work-up.
4) Genetic testing and family screening.
5) Management of left ventricular outflow tract obstruction.
6) Management of symptoms in the absence of obstruction.
7) Atrial arrhythmias.
8) Prevention of SCD.
9) Management of pregnancy.
10)Special issues.
The most important or novel points
What do the guidelines say ?
6. Hypertrophic cardiomyopathy can be caused by
many genetic and non-genetic disorders.
In up to 60% of
patients with HCM,
the disease is an
autosomal
dominant trait
caused by
mutations in
cardiac sarcomere
protein genes.
5-10% of adult cases are caused by other genetic disorders
including inherited metabolic and neuromuscular diseases,
chromosome abnormalities and genetic syndromes.
Etiologic Diagnosis
7. Diagnostic Criteria
Hypertrophic cardiomyopathy is defined by the
presence of increased LV wall thickness that is not
solely explained by abnormal loading conditions.
In an adult, this represents a wall thickness ≥15 mm
in one or more LV myocardial segments(or ≥13 mm
in a first degree relative of someone with HCM)
measured by any imaging technique(echo,CMR or CT)
Patient ≥ 15 mm
FDR ≥ 13 mm
In children : wall thickness ≥ 2 standard deviations above the predicted mean.
8. Diagnostic Work-up
Standard 12-lead ECG and 48-hour ambulatory ECG monitoring
are routinely recommended
Class of recommendation : I
Level of evidence : B
Class of recommendation : I
Level of evidence : B
NSVT
9. Transthoracic echocardiographic
In all patients with HCM at initial evaluation , transthoracic 2D and
Doppler echocardiography are recommended, at rest and during
Valsalva manoeuvre in the sitting and semi-supine positions—and
then on standing if no gradient is provoked.
( Class of recommendation : I Level of evidence : B )
10. In symptomatic patients with a resting or provoked peak
LVOTgradient <50 mm Hg , echo during exercise in the standing,
sitting or semi-supine position is recommended to detect provocable
LVOTO and exercise-induced mitral regurgitation. ( Class I – B )
Exercise stress echocardiography
11. In the absence of contraindications,
CMR with LGE is recommended
in patients with suspected HCM
who have inadequate echo
windows, in order to confirm the
diagnosis.
Class of recommendation : I
Level of evidence : B
Cardiovascular magnetic resonance imaging
With Late Gadolinium Enhancement
HCM with predominately
ventricular septal hypertrophy
(maximal wall thickness, 24 mm)
should be considered in patients who have inadequate
echocardiographic imaging and contraindications for CMR.(IIa - C)
12. Genetic Testing and Family Screening
Genetic testing is recommended in patients fulfilling
diagnostic criteria for HCM, when it enables cascade
genetic screening of their relatives.
Class of recommendation : I Level of evidence : B
13. Management of Left Ventricular Outflow
Tract Obstruction : Medical Treatment
ß-blocker
(Class I-B)
Verapamil
(Class I-B)
Add Disopyramide
(Class I-B)
Diltiazem
(Class IIa-C)
Intolerance or contraindications
Intolerance or contraindications
Digoxin is contraindicated for
the treatment of AF in patients
with obstruction (Class III-C)
15. The indication for septal reduction therapy remains
unchanged in patients with significant obstruction
(baseline or provoked gradient > 50 mmHg) and
moderate-to-severe symptoms (NYHA functional class III-
IV) or recurrent exertional syncope despite maximum
tolerated medical therapy (I-B and IIa-C , respectively).
Septal myectomySeptal alcohol ablation
16. Surgery vs. alcohol ablation
For the first time, septal alcohol ablation is assigned the same
class of recommendation (I-B) as myectomy in expert centers.
The 2 procedures have similar efficacy and complications rates.
Septal alcohol ablation has a higher rate of atrioventricular block
than surgery (12% vs 5%).
Septal myectomy, rather than septal
alcohol ablation, is recommended in patients
with an indication for septal reduction therapy
and other lesions requiring surgical intervention
(e.g. mitral valve repair/replacement, papillary
muscle intervention). (Class I-C)
17. Dual chamber pacing to reduce LVOTO
Permanent AV sequential pacing with optimal AV
interval may be considered in symptomatic adult
patients who are unsuitable for—or unwilling to
consider—other invasive septal reduction
therapies,and in patients who require an ICD (IIb-C)
LVOTO is abolished70 mmHg
18. Management of symptoms in the absence of
obstruction
Heart failure NYHA functional Class II–IV
and preserved LV ejection fraction (≥50%)
& no evidence for resting or provocable LVOTO
ß-blockers, verapamil or Diltiazem
( class IIa- C )
Low-dose loop and thiazide Diuretics
( class IIa-C )
19. Heart failure and reduced LV ejection
fraction (< 50%) & no evidence for
resting or provocable LVOTO
ß-blocker + ACEI (or ARB if ACEI not tolerated) ( Class IIa - C )
Low-dose loop diuretics ( Class IIa -C )
Mineralocorticoid receptor antagonist ( Class IIa - C )
Digoxin for Heart Rate Control in Patients With Atrial Fib (Class IIb- C )
Management of symptoms in the absence of
obstruction
is recommended in patients in NYHA functional class II-IV, LV
ejection fraction < 50%, a QRS duration > 120 ms, and LBBB (ClassIIa-C).
20. Atrial fibrillation is the most common arrhythmia in patients
with HCM.
New-onset AF is frequently associated with heart failure
symptoms and so should be treated promptly in accordance
with ESC guidelines.
Atrial tachyarrhythmia
21. Atrial fibrillation
Patients with HCM and paroxysmal,
persistent or permanent AF should receive
treatment with vitamin K antagonists.
(Class I-B)
Lifelong therapy with oral anticoagulants is
recommended, even when sinus rhythm is
restored. (Class I-C)
Patients in sinus rhythm with LA diameter
≥45 mm should undergo 6–12 monthly
48-hour ambulatory ECG monitoring to
detect AF. (Class IIa-C)
CHA2DS2-VASc
score is not
recommended
Warfarin for all
22. Prevention of sudden cardiac death
Model for estimating sudden cardiac death risk
The HCM Risk-SCD formula is as follows:
Probability = 1 – 0.998
where = [0.15939858 x maximal wall thickness
(mm)] - [0.00294271 x maximal wall thickness² (mm²)] +
[0.0259082 x left atrial diameter (mm)] + [0.00446131 x maximal
(rest/Valsalva) left ventricular outflow tract gradient (mm Hg)] +
[0.4583082 x family history SCD] + [0.82639195 x NSVT] +
[0.71650361 x unexplained syncope] - [0.01799934 x age at clinical
evaluation (years)].
SCD at 5 years
exp (Prognostic index)
The formula is available online
European Society of Cardiology. HCM Risk-SCD Calculator. 2014.
Available at:www.doc2do.com/hcm/webHCM.html
23.
24. Prevention of sudden cardiac death : ICD
Secondary Prevention :
ICD implantation is recommended in patients who have
survived a cardiac arrest due to VT or VF (Class I-B)
Primary Prevention :
Estimate the 5-year risk of SCD using the HCM Risk-SCD model
HIGH RISK
5 – year risk ≥6%
INTERMEDIATE RISK
5 – year risk ≥4 - <6%
LOW RISK
5–year risk <4%
ICD should be considered
( Class IIa – B )
ICD may be considered
( Class IIb-B )
ICD generally not indicated
(Class III-B)
25. Management of pregnancy
HCM Women : Ideally, risk assessment should be
performed before conception,using the modified
WHO classification.
26. Modified WHO classification of maternal cardiovascular risk
Application to HCMRisk of pregnancyRisk
class
-of
maternal mortality and no/mild
risk of morbidity
I
Most women with HCM:
mild to moderate LVOTO;
asymptomatic with or without
medication, well-controlled
arrhythmia, normal systolic LV
function or mild LV dysfunction
of maternal
mortality or moderate increase
in morbidity
II
Severe LVOTO, symptoms or
arrhythmias despite optimal
medication, moderate systolic LV
dysfunction
of
maternal mortality or severe
morbidity
III
Severe systolic LV dysfunction, severe
symptomatic LVOTO
of maternal
mortality or severe morbidity;
pregnancy contraindicated
IV
Yes
No
27. Recommendations on reproductive issues in women with HCM
β-Blockers (preferably metoprolol) should be started in women
who develop symptoms during pregnancy. ( Class I - C )
β-Blockers (preferably metoprolol) should be continued in women
who used them before pregnancy. (Class IIa - C )
Therapeutic anticoagulation with LMWH or vitamin K
antagonists depending on the stage of pregnancy is
recommended for atrial fibrillation. (Class I - C )
Cardioversion should be considered for persistent atrial
fibrillation. (Class IIa - C)
28. SPECIAL ISSUES
The last section of the guideline discusses several
scenarios requiring special considerations in the
diagnosis and management of HCM.
This section discusses the differential diagnosis between
HCM and the normal training effect in athletes or
hypertensive heart disease
29. Clinical features that assist in the differential diagnosis of
hypertensive heart disease and hypertrophic cardiomyopathy
Clinical features favouring hypertension only
Normal 12 lead ECG or isolated increased voltage
without repolarisation abnormality
Regression of LVH over 6–12 months tight systolic
blood pressure control (<130 mm Hg)
Clinical features favouring HCM
Family history of HCM
Right ventricular hypertrophy
Late gadolinium enhancement at the RV insertion points
or localized to segments of maximum LV thickening on CMR
Maximum LV wall thickness ≥15 mm (Caucasian); ≥20 mm (black)
Severe diastolic dysfunction
Marked repolarisation abnormalities, conduction disease
or Q-waves on 12 lead ECG
30. Web Table 7:
Clinical features that favour the diagnosis of hypertrophic cardiomyopathy in
elite athletes with maximal left ventricular wall thickness 12–15 mm
(Level of Evidence B or C )
Hypertrophic
CardiomyopathyAthlete’s Heart
The challenge : “Grey Zone” of left ventricular wall thickness 12–15 mm
How to differentiate athlete’s heart from HCM ?
31. ASH (septal to posterior wall thickness ≥1.5)
Complete SAM of mitral valve
LV end diastolic diameter <45 mm
Late gadolinium enhancement on CMR
Resting intraventricular gradient
Incomplete SAM of mitral valve
LVH of the anterior septum or the posterior wall ≥12 mm
Left atrium >45 mm
RVH (right ventricular subcostal thickness >5 mm)
Myocardial crypts identified with CMR
Mitral inflow pattern E < A(20 years old)
Tissue Doppler Imaging: Ea <9 cm/sec
Tissue Doppler Imaging: Sa <9 cm/sec
Increased BNP
Ea 10–13 cm/sec
Diastolic radial strain <7 cm/sec
VO2max <50ml/kg/min or <120% of predicted VO2max
Increased left ventricular torsion
Structural
Functional
Features favouring HCM in Athlete’s
32. Abnormal Q waves in at least two leads from II, III, aVF (absence of left
anterior hemiblock), V1–V4, I, aVL, V5–V6
Inverted T –waves in two or more leads from lead groups II, III, aVF or/and
I, aVL,V5-V6
Inverted T–waves V2-V4 (>16 years old)
Giant negative T–waves in two contiguous leads (> 5mm)
Inverted T–waves in leads V2–V4 (<16 years old)
Complex ventricular arrhythmias at 24 h Holter rhythm recording or >2000
PVCs/24 h
Family history of HCM in first degree relative(s)
Female gender
Family history of SCD in first degree relative(s) ≤40 years
Cardiovascular symptoms (unexplained syncope,
disproportionate dyspnoea on exertion, chest pain, palpitations)
No response to detraining for 3 months
Disease causing sarcomere mutationGenetics
Detraining
ECG
Demographics
Features favouring HCM in Athlete’s
33. The ESC guideline on the
diagnosis and management
of HCM is the most recent
update on the topic.
The most important points of
the guideline refer to the
etiologic diagnosis of HCM,
genetic testing, structured
management of LVOTO, atrial
arrhythmias, and SCD
prevention.
Conclusion