This document discusses chronic coronary syndrome (CCS), previously known as stable coronary artery disease. It defines CCS and outlines the six entities it can be classified into. It discusses the natural history, pathophysiology, risk factors, diagnosis and management of CCS. Key changes from 2013 guidelines include exercise stress testing now recommended for assessing symptoms and risk rather than diagnosis, and several new second-line treatment options for angina added based on heart rate, blood pressure and tolerance. Invasive testing guidelines were also updated.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.The incidence of WPW is between 0.1% and 0.3% in the general population.Sudden cardiac death in people with WPW is rare (incidence of less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the abnormal accessory pathway.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.The incidence of WPW is between 0.1% and 0.3% in the general population.Sudden cardiac death in people with WPW is rare (incidence of less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the abnormal accessory pathway.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supra-ventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
ventricular premature complexes and idioventricular rhythm identification is important in the ICU ..they may run into arryhthmias..look over my seminar...
any queries...
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supra-ventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
ventricular premature complexes and idioventricular rhythm identification is important in the ICU ..they may run into arryhthmias..look over my seminar...
any queries...
Angina also known as angina pectoris is a medical condition characterized by chest pain usually left sided due to inadequate blood supply (ischemia) to the heart muscles due to obstruction (like presence of blood clot), narrowing or contraction (vasospasm) of the supplying coronary arteries.
Angina pectoris is a clinical syndrome usually characterized by episodes of pain or pressure in the anterior chest . The cause is usually insufficient coronary blood flow which results in a decreased oxygen supply to meet an increased myocardial demand for oxygen in response to physical exertion or emotional stress.
also known as heart disease. this topic describe the heart caused impaired coronary blood flows. what are the symptoms and how nurses handled it also the diagnostic test to confirm and the medicine
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
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.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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.
2. Introduction
▪ Coronary Artery Disease(CAD) is the most common cause of
angina. It is a pathological process characterized by
atherosclerotic plaque accumulation in the epicardial arteries,
whether obstructive or non-obstructive.
▪ Ischemic Heart Disease(IHD) is a condition in which the is an
inadequate supply of blood and oxygen to portion of the
myocardium associated with disturbance in myocardial function
▪ Occult CAD is common in those who present with other forms of
atherosclerotic vascular disease, such as intermittent claudication
or stroke
6. 1772 William Heberden
he described angina as
some account of the
disorder of breast
Later Royal College of Physicians
in London named it as Angina
Pectoris
7. Angina Pectoris
▪Angina pectoris is a symptom
complex caused by transient
myocardial ischemia, which occurs
whenever there is an imbalance
between myocardial oxygen supply
and demand.
9. Chronic Coronary Syndrome
▪ The 2019 ESC Guidelines replace the term
“Stable CAD” with Chronic Coronary Syndrome.
▪ This implies that CAD is a dynamic process, the
clinical presentation of which can be either acute
or chronic
▪ The CCS syndromes have been classified in to six
entities…
10. Suspected and established CCS are-
▪ 1.Patients with suspected CAD and stable angina symptoms, and/or
dyspnea.
▪ 2.Patients with new onset of HF or LV dysfunction and suspected CAD.
▪ 3.Asymptomatic and symptomatic patients with stabilized symptoms < 1
year after an ACS or patients with recent revascularization.
▪ 4.Asymptomatic and symptomatic patients >1 year after initial diagnosis
or revascularization
▪ 5.Patients with angina and suspected vasospastic or microvascular
disease
▪ 6.Asymtomatic subjects in whom CAD is detected at screening.
14. History and risk factors( A careful history is the cornerstone of
the diagnosis of angina)
The history should include any manifestation of CVD and risk
factors…
Family history of CVD
Dyslipidemia
Diabetes
Hypertension
Smoking &
Other lifestyle factors
15. The characteristics of Angina
Location Chest, near the sternum, but may be felt anywhere from the
epigastrium to the lower jaw or teeth, between the shoulder
blades, or in either arm to the wrist and fingers.
Character The discomfort is often described as pressure, tightness or
heaviness; sometimes strangling, constricting or burning.
Duration The duration of the discomfort is brief less than 10 mins in
the majority of cases, and more commonly just a few
minutes or less and chest pain lasting for seconds is unlikely
to be due to CAD.
Relationship to exertion
and other exacerbating
or relieving factors
Become more severe with increased levels of exertion.
16. Clinical Classification of Suspected Anginal
Symptoms
Typical Angina
Meets the following three characteristics:
1.Constricting discomfort in the front of the chest or in the
neck, jaw, shoulder or arm.
2.Precipitated by physical exertion
3.Relieved by rest or nitrated within 5 mins
Atypical
angina
Meets two of these characteristics.
Non-anginal
chest pain
Meets only one or none of these characteristics
17. Canadian Cardiovascular Society
Grade Description of anginal severity
I Angina only with Strenuous
exertion
Presence of angina during strenuous, rapid or prolonged ordinary
activity(walking or climbing the stairs)
II Angina with moderate Slight limitation of ordinary activities when they are performed rapidly,
after meals, in clod , in wind under emotional stress or during the first few
hours after waking up, but also walking uphill, climbing more than one
flight of ordinary stairs at a normal pace, and in normal conditions,
III Angina with mild exertion Having difficulties walking one or two blocks or climbing one flight of stairs,
at normal pace and conditions
IV Angina at rest No exertion needed to trigger angina.
20. Investigations(Class I)
Biochemical Test:
▪ CBC
▪ Fasting plasma glucose and HbA1c
▪ Lipid profile
▪ Serum creatinine and eGFR
▪ Serum uric acid test
▪ Thyroid function test
▪ Troponin levels(Only in suspected Patient)
21. Resting ECG
▪ Even in typical angina chest pain half the patient may not have any classical
changes.
▪ A resting 12 lead ECG is recommended in all patients with chest pain without
an obvious non-cardiac cause (Class I Level C).
▪ A resting 12 lead ECG is recommended in all patients during or immediately
after an episode of angina suspected to be indicative of clinical instability of
CAD (Class I Level C).
▪ Ambulatory ECG monitoring is recommended in patients with chest pain and
suspected arrhythmias(Class I Level C).
22. Echocardiography(Class I level B)
A resting transthoracic echocardiogram is recommended in all
patients for:
1. Exclusion of alternative causes of angina
2. Identification of regional wall motion abnormalities suggestive of
CAD
3. Measurement of LVEF for risk stratification
4. Evaluation of diastolic dysfunction
23. Chest X-Ray
▪Chest X-ray is recommended for
patients with a typical presentation,
signs and symptoms of HF, or suspicion
of pulmonary disease(Class I level C).
24. Exercise ECG
▪ Exercise ECG is recommended for the assessment of exercise
tolerance, symptoms, arrhythmias, BP response, and event risk in
selected patients(class I level C)
▪ Exercise ECG is not recommended for diagnostic purpose in
patients with ≥ 0.1 mV St- segment depression on resting ECG
or who are being treated with digitalis(class III level C)
25. Functional non invasive tests
▪Stress Echocardiography
▪Single photon emission CT(SPECT)
▪Positron emission tomography(PET)
▪Myocardial contrast echocardiography or
contrast CMR
31. Lifestyle recommendations for patients with
chronic coronary syndromes
Smoking cessation Use pharmacological and behavioural strategies to help patients quit smoking. Avoid
passive smoking
Healthy diet Diet high in vegetables, fruit, and wholegrains. Limit saturated fat to ,10% of total intake.
Limit alcohol to ,100 g/wk or 15 g/day
Physical activity 30 - 60 min moderate physical activity most days, but even irregular activity is beneficial.
Healthy weight Obtain and maintain a healthy weight (<25kg/m2), or reduce weight through
recommended energy intake and increased physical activity.
Other Take medications as prescribed. Sexual activity is low risk for stable patients not
symptomatic at low-to-moderate activity levels
32. Healthy Diet characteristics
▪ Increase consumption of fruits and vegetables(>200gm each day).
▪ 35-45 gm of fibers per day, preferably from whole grains.
▪ Moderate consumption of nuts(30 gm/day, unsalted).
▪ 1-2 servings of fish per week(one to be oily fish).
▪ Limited lean meat, low fat dairy products, and liquid vegetables oils.
▪ Saturated fats to account for <10% of total energy intake; replace with poly unsaturated
fats.
▪ As little intake of trans unsaturated fats as possible, preferably no intake from processed
food, and <1% of total energy intake.
▪ 5-6 gm salt per day.
▪ If alcohol is consumed, limiting intake to <100 gm/wk or <15 gm/day is recemented.
▪ Avoid energy-dense foods such as sugar-sweetened soft drinks.
35. Nitrates:
▪ Nitrates act directly on vascular smooth muscle to produce venous
and arteriolar dilatation.
▪ They help angina by lowering preload and afterload, which reduces
myocardial oxygen demand and by increasing myocardial oxygen
supply through coronary vasodilatation.
▪ No mortality benefit or cannot prevent heart attack.
▪ Short acting nitrates for acute effort angina: Sublingual and spray
nitroglycerin formulations provide immediate relief of effort angina
▪ Long acting nitrates for angina prophylaxis.
36. Beta Blockers
▪ These lower myocardial oxygen demand by
reducing heart rate, BP and myocardial
contractility.
▪ Discontinuation should be tapered and not
abrupt.
▪ The principal side effects of beat blockers are
fatigue, depression, bradycardia, heart block,
bronchospasm, peripheral vasoconstriction,
postural hypotension, impotence and masking of
hypoglycemia symptoms.
38. Potassium Channel Activator
▪Nicorandil(10-30 mg twice daily orally) is a
nitrate derivatives of nicotinamide, with
antianginal effects similar to those of
nitrates or beta blockers.
▪Side effects include nausea, vomiting and
potentially severe oral, intestinal and
mucosal ulcerations
39. If channel antagonists
▪Ivabradine is the first of this class of drug.
▪It does not inhibit myocardial contractility
and appear to be safe in patients with heart
failure.
▪It includes bradycardia by modulating ion
channel in the sinus node.
40. Ranolazine
▪Is a selective inhibitor of the late inward
sodium current in coronary artery smooth
muscle cell, with a secondary effect on
calcium flux and vascular tone, reducing
anginal symptoms.
▪Side effects include dizziness, nausea,
constipation, Qt prolongation.
41. Trimetazidine
▪ Trimetazidine is an anti-ischemic(anti-anginal)
metabolic agent, which improves myocardial
glucose utilization through inhibition of fatty acid
metabolism, also known as fatty acid oxidation
inhibitor.
▪ It is contraindicated in Parkinson`s disease and
motion disorders, such as tremor(shaking),
muscle rigidity, walking disorders and restless leg
syndrome.
42. Event Prevention
Recommendations Class level
Aspirin 75-100 mg daily is recommended in patients with a previous MI or
revascularization
I A
Clopidogrel 75 mg daily is recommended as an alternative to aspirin in patients with
aspirin intolerance
I B
44. ACE inhibitors
▪ACE inhibitors or ARBs are
recommended if a patient has
other conditions (e.g. Heart
failure, Hypertension or diabetes)
45. Statins
Recommendation Class Level
Statins are recommended in all patients with CCS. I A
If a patient`s goal is not achieved with the maximum tolerated dose of statin, combination
with ezetimibe is recommended.
I B
For patients at very high risk who do not achieved their goal on a maximum tolerated dose
of statin and ezetimibe, combination with PCSK9 inhibitor is recommended.
I A
49. Revascularization
▪ In patients with CCS, optimal medical therapy is key for reducing
symptoms, halting the progression of atherosclerosis and
preventing atherothrombotic events,
▪ Myocardial revascularization plays a central role in the
management of CCS on top of medical treatment, but always as
an adjunct to medical therapy without supplanting it.
▪ Revascularization by PCI or CABG may effectively relieve angina,
reduce the use of antianginal drugs and improve exercise capacity
and quality of life compared with a strategy of medical therapy
alone.
50. 2013 vs 2019
Changes in major recommendations
2013 class class
Exercise ECG is recommended as the initial test to
establish a diagnosis of stable CAD in patients
with symptoms of angina and intermediate PTP of
CAD , free of anti-ischemic drugs, unless they
cannot exercise or display ECG changes that
make the ECG non-evaluable.
I Exercise ECG is recommended for the assessment of
exercise tolerance, symptoms, arrhythmias, BP
response, and event risk in selected patients.
I
Exercise ECG may be considered as an alternative
test to rule-in or rule-out CAD when other non-
invasive or invasive imaging methods are not
available.
IIb
Exercise ECG should be considered in patients on
treatment to evaluate control of symptoms and
ischemia
IIa Exercise ECG may be considered in patients on
treatment to evaluate control of symptoms and
ischemia.
IIb
For second-line treatment it is recommended that
long acting nitrates, ivabradine, nicorandil, or
ranolazine are added according to heart rate, BP,
and tolerance.
IIa Long-acting nitrates should be considered as a
second-line treatment option when initial therapy
with a beta-blocker and/or a non DHP-CCB is
contraindicated, poorly tolerated, or inadequate in
controlling angina symptoms.
IIa
51. 2013 vs 2019
Changes in major recommendations
2013 class class
For second-line treatment, trimetazidine may be
considered,
IIb Nicorandil, ranolazine, ivabradine, or trimetazidine
should be considered as a second-line treatment to
reduce angina frequency and improve exercise
tolerance in subjects who cannot tolerate, have
contraindications to, or whose symptoms are not
adequately controlled by beta-blockers, CCBs, and
long-acting nitrates.
IIa
In selected patients, the combination of a beta-
blocker or a CCB with second-line drugs (ranolazine,
nicorandil, ivabradine, and trimetazidine) may be
considered for first-line treatment according to heart
rate, BP, and tolerance.
IIb
53. 2013 vs 2019
Changes in major recommendations
2013 class class
In patients with suspected coronary microvascular
angina: intracoronary acetylcholine and
adenosine with Doppler measurements may be
considered during coronary arteriography, if the
arteriogram is visually normal, to assess
endothelium-dependent and non-endothelium-
dependent CFR, and detect
microvascular/epicardial vasospasm.
IIb Guidewire-based CFR and/or microcirculatory
resistance measurements should be considered in
patients with persistent symptoms, but coronary
arteries that are either angiographically normal or
have moderate stenoses with preserved iwFR/FFR.
IIa
Intracoronary acetylcholine with ECG monitoring
may be considered during angiography, if coronary
arteries are either angiographically normal or have
moderate stenoses with preserved iwFR/FFR, to
assess microvascular vasospasm
IIb
54. 2013 vs 2019
Changes in major recommendations
2013 class class
In patients with suspected coronary microvascular
angina: transthoracic Doppler echocardiography
of the LAD, with measurement of diastolic
coronary blood flow following intravenous
adenosine and at rest, may be considered for non-
invasive measurement of CFR.
IIb Transthoracic Doppler of the LAD, CMR, and PET
may be considered for non-invasive assessment of
CFR.
IIb
