Category Archives: students & professionals

Top 10 Cardiology Articles of the week

Top 10 Cardiology Articles of the week  (24.11.14 – 30.11.14)

1. Transcatheter Closure of Large Atrial Septal Defects: Feasibility and Safety in a Large Adult and Pediatric Population

Conclusions—Closure of large atrial septal defects using the Amplatzer device is safe and effective in both adults and children. Superior and posterior rim deficiencies are associated with procedural failure. Closure can be performed under transthoracic  echocardiographic guidance in experienced centers. Early device migration is rare and can be safely managed by device extraction.  Long-term follow-up showed no deaths or major late complications in  311 patients.

2. Stent Coverage and Neointimal Proliferation in Bare Metal Stents Postdilated With a Paclitaxel-Eluting Balloon Versus Everolimus-Eluting Stents: Prospective Randomized Study Using Optical Coherence Tomography at 6-Month Follow-Up

Conclusions—Good stent strut coverage of >94% was found in both therapy groups. Despite greater suppression of global neointimal growth in DES, both DES and BMS+DEB effectively prevented clinically relevant focal restenosis at 6-month follow-up.

3. Multicenter Evaluation of a Next-Generation Balloon-Expandable Transcatheter Aortic Valve
Conclusions – This third-generation device addresses major deficiencies of earlier valves in terms of ease of use, accuracy of positioning, and paravalvular sealing. The rates of mortality and stroke with transfemoral access are among the lowest reported and support further evaluation as an alternative to open surgery in intermediate-risk patients.
(Safety and Performance Study of the Edwards SAPIEN 3 Transcatheter Heart Valve [SAPIEN3]; NCT01808287)

4. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation

5. Percutaneous Left Atrial Appendage Closure: Procedural Techniques and Outcomes

6. Atenolol versus Losartan in Children and Young Adults with Marfan’s Syndrome

Conclusion – Among children and young adults with Marfan’s syndrome who were randomly assigned to losartan or atenolol, no significant difference was found in the rate of aortic-root dilatation between the two treatment groups over a 3-year period.

7. Inactivating Mutations in NPC1L1 and Protection from Coronary Heart Disease

Conclusion – Naturally occurring mutations that disrupt NPC1L1 function were found to be associated with reduced plasma LDL cholesterol levels and a reduced risk of coronary heart disease.

8. MagnaSafe: MRI safe for patients with pacemakers, ICDs

9. Catheter Ablation of Atrial Fibrillation in Patients with Left Ventricular Systolic Dysfunction: A Systematic Review and Meta-Analysis

10. Long-term Clinical and Angiographic Outcomes of the Mini-STAR Technique as a Bailout Strategy for Percutaneous Coronary Intervention of Chronic Total Occlusion

PARADIGM-HF Trial

A new class of drug (Neprilysin inhibitor ) when combined with angiotensin receptor blocker , has been shown to be better than Enalapril.

Angiotensin–Neprilysin Inhibition versus Enalapril in Heart Failure — NEJM.

Extended-Release Niacin with Laropiprant

HPS2-THRIVE trial

Among patients with atherosclerotic vascular disease, the addition of extended-release niacin–laropiprant to statin-based LDL cholesterol–lowering therapy did not significantly reduce the risk of major vascular events but did increase the risk of serious adverse events.  

Effects of Extended-Release Niacin with Laropiprant in High-Risk Patients — NEJM.

cpr

Sudden cardiac death

What is sudden cardiac death (SCD) ?

Sudden cardiac death is defined as natural death from cardiac causes, heralded by abrupt loss of consciousness within 1 hour of the onset of an
acute change in cardiovascular status. Related terms are sudden cardiac arrest and cardiovascular collapse. Sudden cardiac arrest means abrupt cessation of cardiac
mechanical function, which may be reversed by prompt intervention but will lead to death in its absence. Cardiovascular collapse means sudden loss of effective
blood flow due to cardiac and/or peripheral vascular such as cardiac arrest or syncope.

What is the relation to heart disease?

preexisting heart disease may or maynot have been known to be present. The mode of death is natural rapid and unexpected.

What are the symptoms?

Prodromes occuring weeks or months before an event are not very accurate to predict SCD. Sudden onset of chest pain, dyspnea, palpitation, lightheadedness
often precede the onset of cardiac arrest and eventual death.

How big is the problem?

For an adult population 35 years of age and older, the overall incidence of sudden cardiac death is 0.1% to 0.2% per year (that means in a country like India
12,00,000 to 24,00,000 people die suddenly from natural cardiac causes each year). Among people who have disease of coronary arteries of heart around 50% die
suddenly and unexpectedly. Even in developed countries where there is a decrease in total number of deaths due to coronary artery disease, the proportion of
deaths that are sudden and unexpected has remained same. These examples highlight the extent of the problem.

Who are at increased risk?

The conditions increasing the risk of sudden cardiac death are

  1. Coronary artery disease- Myocardial infarction, Angina etc
  2. Myocardial diseases and heart failure- e.g. dilated cardiomyopathy, ischemic cardiomyopathy etc
  3. Hypertrophy of ventricular myocardium – hypertrophic cardiomyopathy, left ventricular hypertrophy due to hypertension, etc
  4. Inflammatory diseases of heart- viral myocarditis, sarcoidosis, amyloidosis,
  5. Arrhythmogenic right ventricular dysplasia
  6. Diseases of cardiac valves- Aortic stenosis/insufficiency, mitral valve prolapse
  7. Electrical diseases of heart – long QT syndrome, Brugada syndrome, idiopathic ventricular fibrillation etc.
Mechanism of Sudden death

In 80% of cases sudden cardiac death is caused by ventricular tachycardia (VT) or ventricular fibrillation (VF) and in 20% of cases
SCD is caused by bradycardia. Patients having tachycardia have a relatively better outcome and chances of survival than those having bradycardia.

Management

The acute management of cardiac arrest is cardiopulmonary resusitation. More information about latest guidelines of CPR can be found
here

Prevention

Prevention of SCD is divided into two parts: Secondary prevention and Primary prevention. Secondary prevention means preventing further cardiac arrest
in people who have survived one cardiac arrest. Primary prevention means preventing cardiac arrest in people who have rish factors for cardiac arrest
but so far haven’t suffered a cardiac arrest.
Implantable cardioverter-defibrillator(ICD) is a device shown to be effective in secodary and primary prevention of SCD. This device is implanted like
a pacemaker and it gives an electrical shock from inside of the heart to abort an episode of VT or VF. It also has pacing function to support when the
heart rate falls.
Clinical trials like AVID, CASH, CIDS have shown effectiveness of ICD in secondary prevention of SCD. Clinical trials like MADIT, CABG-Patch, MUSTT, DEFINITE and
SCD-HeFT have shown benefit odf ICD in SCD.
Many modifications of the device has come like- subcutaneous ICD and wearable ICD.

Electrophysiological study
EPS and radiofrequency ablation can be done in selected patients to prevent further episodes of cardiac arrest.

Summary: sudden cardiac death is a devastating event resulting in rapid, unexpected and natural death due to cardiac causes. It can occur in persons
with known or unknown heart disease. Effective therapies are available. Increasing awareness about the condition and early therapy can result in
reduction of risk of sudden cardiac death
Keyword: Sudden cardiac death, sudden cardiac arrest, implantable cardioverter defibrillator (ICD), coronary artery disease, heart failure, heart disease, cardiology.

Implantable cardioverter defibrillator (ICD) – the others

Implantable cardioverter defibrillator (ICD) – the others

New ACC/AHA/HRS Expert consensus document for implantable cardioverter defibrillator (ICD) implantation in patients who are excluded or not well represented
in clinical trials.

A guideline has been published for ICD implantation. This new document is a good attempt at helping cardiologists in deciding about ICD.
There are some good points about the document.

Overview of the guideline:

1. The doument considers the published studies in ICD and makes recommendations.
2. Since the guideline considers only patients who are excluded or not well represented in clinical trials, there is no class of recommendations or level of evidence.
Rather there are categories like recommended, not recommended, can be done etc
3. Patients have been divided into different populations and recommendations are made for each patient population.

The broad categories considered are:

1. ICD Implantation in the Context of an Abnormal Troponin that Is Not Due to a Myocardial Infarction
2. ICD Implantation Within 40 Days of a Myocardial Infarction
3. ICD Implantation Within 90 Days of Revascularization
4. ICD Implantation <9 Months from the Initial Diagnosis of Nonischemic Cardiomyopathy

We will discuss the recommendations in each category

1. ICD Implantation in the Context of an Abnormal Troponin that Is Not Due to a Myocardial Infarction

First group of patients are those having elevated troponin levels but not fulfilling the  definition of MI (see other causes of elevated troponin e.g.kidney disease,
acute pulmonary embolus, heart failure, myocarditis, chest trauma, or tachyarrhythmia)and satisfying standard ICD indications for primary and
secondary prevention. ICD is recommended is such patients.
The idea is to define whether the elevated cardiac markers are due to MI or not. If not due to MI then go for ICD implatation early and no need to wait
for 40 days, like in a post MI setting.

2. ICD Implantation Within 40 Days of a Myocardial Infarction

 

1-Implantation of an ICD within the first 40 days following acute MI in patients with                       preexisting systolic ventricular dysfunction (who would have qualified for a
primary prevention ICD) is not recommended.
2-In patients who, within 40 days of an MI, require nonelective permanent pacing, who               also would meet primary prevention criteria for implantation of an ICD, and recovery of       left ventricular function is uncertain or not expected, implantation of an ICD  is                          recommended.
The basis of such recommendations has been explained by the writing group
“This reflects the fact that implantation of
a pacemaker or ICD is associated with some risk, especially
infection. If the likelihood that a patient requiring PPM implantation
early post-MI will ultimately require a second
procedure to extract the PPM and leads and replace it with
an ICD system 40 days later, it would seem inappropriate
not to implant an ICD rather than a PPM.”
3-Patients within 40 days of an MI who subsequently present sustained or hemodynamically significant ventricular tachyarrhythmias.

In this scenario the following recommendations are made
(i)In patients who, within 40 days of an MI, develop sustained (or hemodynamically significant) ventricular tachyarrhythmias >48 hours after an MI and
in the absence of ongoing ischemia, implantation of an ICD is recommended.

(ii)In patients who, within 40 days of an MI, develop sustained (or hemodynamically significant) VT >48 hours after an MI that can be treated by ablation,
implantation of an ICD can be useful.

(iii)In patients who, within 40 days of an MI, develop sustained (or hemodynamically significant) ventricular tachyarrhythmias where there is
clear evidence of an ischemic etiology with coronary anatomy amenable to revascularization (and appropriately treated), implantation
of an ICD is not recommended.
4- Patients within 40 days of MI who present with syncope that is thought to be due to ventricular arrhythmia – implantation of an ICD can be done.
In this recommendation quite a liberal one as there is no need to document ventricular arrhythmia. ICD can be done for suspected ventricular arrhythmia ( on the
basis of clinical history, documented NSVT or EP study). There are no studies that have specifically addressed whether ICD implantation is beneficial  in the setting of syncope thought to be due to a ventricular tachyarrhythmia in the first 40 days after MI. However, the consensus of the writing group is that syncope in the setting of a recent MI is a potentially serious issue, and ICD implantation can be useful if syncope is thought to be due to a ventricular tachyarrhythmia (by clinical history, documented NSVT, or EP study), regardless of timing in relationship to an MI (either <40 days or >40 days after MI).
5- Elective ICD replacement for battery depletion can be done in first 40 days after MI (in patients who have been previously implanted with ICD).
6- ICD implantation in patients within 40 days of an MI who have been listed for heart transplant or implanted with a left ventricular assist device is not recommended.

3. ICD Implantation Within 90 Days of Revascularization.

The ICD indications can be primary and secondary or patients requiring permanent pacing
1-ICD is recommended for primary prevention within 90 days of revascularization
a. In patients who have indication for ICD implantation for primary prevention of sudden cardiac death,and who have undergone revascularization
that is unlikely to result in an improvement in LVEF >0.35, and who are not within 40 days after an acute MI.
2-ICD is recommended for secondary prevention within 90 days of revascularization
a. In patients with abnormal left ventricular function and previous indication for ICD for            secondary prevention of sudden cardiac death (resuscitated from cardiac arrest due to        ventricular tachyarrhythmia) and have abnormal left ventricular function,
implantation of an ICD is recommended.
b. In patients with normal left ventricular function and previous indication for ICD for                  secondary prevention of sudden cardiac death  (resuscitated from cardiac arrest due to        ventricular tachyarrhythmia) that is unlikely related to myocardial ischemia/injury
c. ICD not indicated in patients whose cardiac arrest or VT/VF was due to acute myocardial        ischemia or injury.
3-ICD recommendations for patients with indication for permanent pacemaker

ICD is recommended in patients with indication for permanent  pacemaker + indication for ICD.
This indication is likely to come-up for further discussion in view of recent developments. The FDA has approved Medtronic CRT-D and CRT devices for patients with AV-block,NYHA I,II, III heart failure and LVEF<50% (based on data from BLOCK-HF trial)(http://www.medscape.com/viewarticle/823485).
So many of the patients with the above indication for ICD will receive CRT-D.

4-ICD is recommended in patients who develop  sustained VT/VF not related to myocardial ischemia ,syncope, patients needing pulse generator replacement, patients listed for heart transplant or implanted with ventricular assist devices, who are not within 40 days of acute myocardial infarction

4. ICD Implantation <9 Months from the Initial Diagnosis of Nonischemic Cardiomyopathy

ICD recommended in:
1-Implantation of an ICD for primary prevention is not recommended within the first 3 months after initial diagnosis of NICM.
2-If recovery of left ventricular function is unlikely, implantation of an ICD for primary prevention can be useful between 3 and 9 months after initial diagnosis of NICM.

3-ICD is indicated in patients having sustained VT/VF, syncope, indication for permanent pacing, listed for heart transplant, implanted with ventricular assist devices

Indications for putting an atrial lead:

1. In patients with symptomatic sinus node dysfunction, an atrial lead is recommended.
2. In patients with sinus bradycardia and/or AV conduction disturbances limiting the use and/or up-titration of necessary beta-blocker or other negative chronotropic drug therapy, an atrial lead is recommended.
3. In patients with sinus rhythm who have a documented second- or third-degree AV block, but who are not otherwise candidates for cardiac resynchronization therapy, an atrial lead is recommended.
4. In patients with bradycardia-induced or pause-dependent ventricular tachyarrhythmia (such as patients with long QT syndrome and torsades de pointes) an atrial lead can be useful.
5. In patients with a documented history of atrial arrhythmias (but not in permanent atrial fibrillation), an atrial lead may be considered.
6. In patients with hypertrophic cardiomyopathy and a significant resting or provocable left ventricular outflow tract gradient, an atrial lead may be considered.

Atrial lead not indicated in:

1. In patients with no documented history of atrial arrhythmias who have no other reason for requiring an atrial lead, an atrial lead is not recommended.
2. In patients with permanent or longstanding persistent atrial fibrillation in whom efforts to restore or maintain sinus rhythm are not planned, an atrial lead is not recommended.
3. In patients with conditions likely to result in VF (rather than monomorphic or polymorphic VT) without a bradycardia-induced or pause-dependent mechanism of
initiation and no other indication for an atrial lead, an atrial lead is not recommended. Conditions likely to result in VF – idiopathic ventricular fibrillation, Brugada syndrome, catecholaminergic polymorphous ventricular tachycardia, and short QT syndrome

This article adequately covers patients who really need an ICD, but have been excluded from trials. I have made a simplified version of the document which is easy to
understand. Your comments and questions are welcome

 

 

Note:

1. The diagnostic criteria for acute MI, established by the joint ESC/ACC/AHA/WHF Task  Force, are the following:

An appropriate rise and/or fall in cardiac biomarkers with at
least one value above the 99th percentile upper reference level, together with evidence of myocardial ischemia and with at least ONE of the following:
 1. Electrocardiographic evidence of new ischemia (ST
segment shift or development of left bundle branch
block [LBBB])
2.  Evolution of pathologic Q waves on the electrocardiogram
3.  Imaging evidence of new regional wall motion abnormality
or new loss of viable myocardium
4.  Ischemic symptoms
(J Am Coll Cardiol 2012;60:1581–98.)
2. BLOCK HF trial (N Engl J Med 2013;368:1585-93)

Percutaneous ventricular restoration therapy

Percutaneous ventricular restoration therapy

This is a new form of device therapy for heart failure. The device used is Parachute implant® (http://www.cardiokinetix.com/).

Parachute implant is an umbrella shaped device that is inserted into the left ventricle.

Pathophysiological basis of use:

–          In post MI patients there is progressive LV remodelling (progressive dilatation of the               left ventricle).

–          This dilatation of the ventricle increases the LV wall stress.

wall stress = (LV pressure  × LV diameter)÷  ( 2×LV wall thickness )

–          Increased LV wall stress increases LV afterload

–          Increased LV afterload worsens the LV dysfunction.

What the device does:

This device is useful in patients with old anterior and antero-apical infarctions and LV             dysfunction.

–          Parachute implant separates the dilated apical portion of the left ventricle from the                 normally contracting LV.

–          There by improves the LV geometry

–          Reduces the LV afterload

–          Improves LV function

Data regarding efficacy:

In a recent study presented at ESC heart failure congress,

–          There was a significant reduction in LV end-diastolic (120.8 vs 103.8) an end-systolic volumes (87.6 vs 73.2) at 12 months after parachute implant. There was significant increase in LVEF (28.4 vs 30.4).

–          Symptomatic improvement

–          Improvement in functional class

–          It might improve heart failure related admissions and mortality.

Risks:

–          Interference of the device with papillary muscles or apical chordae tendineae is unknown

–          Risks and consequences of dislocation.

–          Thrombo-embolic risk.

Ongoing Trials:

PARACHUTE IV

 Conclusion:

This device represents a percutaneous alternative for LV reduction surgeries. Long term safety and efficacy results to be seen.

APPROACH TO SYNCOPE

APPROACH TO SYNCOPE
History taking in cardiology cont.
Syncope has been defined by the European society of cardiology as “A transient loss of consciousness due to transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous recovery.”
Syncope is a common problem, it causes significant agony and apprehension and may result in serious injury to the patient. Analysing and making an etiologic diagnosis of syncope is a difficult problem and even after investigations a significant number of patients still remain unexplained.
A detailed history is of paramount importance in the evaluation of syncope. Because all evaluation is usually retrospective. We will discuss in this article an approach to syncope and how to make a probable diagnosis from history.

STEPS IN THE EVALUATION OF SYNCOPE:
Patients present with the complain of loss of consciousness. From here we have to proceed in a systematic fashion to make a diagnosis. We will approach syncope under two headings
1. Taking the history of the episode
2. Analysing the history to reach at a diagnosis

RECORDING THE HISTORY OF SYNCOPE:

Below is a sample questionnaire for recording the history
WHAT WERE THE CIRCUMSTANCES JUST PRIOR TO THE ATTACK?

• The physical position of the patient is important. Inquire whether the patient was supine, sitting or standing.

• Activity related to syncope episode (rest. change in posture, during or after exercise, during or immediately after urination, defecation cough, or swallowing)
• Predisposing factors (e.g. crowded or warm places, prolonged standing. post-prandial period) and of precipitating events (e.g. fear, intense pain, neck movements)

HOW THE ATTACK STARTED ?
• Nausea, vomiting, abdominal discomfort, feeling of cold, sweating, aura, pain in neck or shoulders, blurred vision, dizziness
• Palpitations

QUESTIONS ABOUT THE ATTACK (EYEWITNESS)
• Way of falling (slumping or kneeling over), skin color (pallor, cyanosis, flushing), duration of loss of consciousness, breathing pattern (snoring) movements (tonic, clonic, tonic-clonic, minimal myoclonus or automatism), duration of movements, onset of movement in relation to fall, tongue biting
HOW THE ATTACK ENDED?
• Nausea, vomiting, sweating, feeling of cold, confusion, muscle aches, skin color, injury, chest pain, palpitations, urinary or fecal incontinence
BACKGROUND HISTORY OF THE PATIENT
• Family history of sudden death, congenital arrhythmogenic heart disease or fainting
• Previous cardiac disease
• Neurological history (Parkinsonism, epilepsy, narcolepsy)
• Metabolic disorders (diabetes, etc.)
• Medication (antihypertensive, antianginal, antidepressant agent, antiarrhythmic, diuretics, and QT-prolonging agents) or other drugs including alcohol
• In the case of recurrent syncope, information on recurrences such as the time from the first synopal episode and on the number of spells

ANALYSIS OF HISTORY
Once the history is recorded, the next step is to differentiate syncope from other causes of transient loss of consciousness.
Causes of transient loss of consciousness (T-LOC)

1. Syncope – we will discuss
2. Neurologic or cerebrovascular disease – e.g. seizure, posterior circulation TIA
3. Metabolic syndromes and coma – e.g. hypoglycaemia, drug or alcohol intoxication, hypoxia, hypocapnea
4. Psychogenic syncope- anxiety disorders, panic disorders, somatization disorders
DIFFERENTIATING SYNCOPE FROM OTHER CAUSES OF T-LOC
Following questions help in differentiating syncope from other causes of T-LOC
(1) Did the patient experience a complete loss of consciousness?
(2) Was the loss of consciousness transient with rapid onset and short duration?
(3) Did the patient recover spontaneously, completely, and without sequelae?
(4) Did the patient lose postural tone?
If the answer to one or more of these questions is negative, other nonsyncopal causes (as listed above) of transient loss of consciousness should be evaluated.
ESTABLISHING THE CAUSE OF SYNCOPE
Features of some of the common causes of syncope

Neutrally mediated syncope Arrhythmia Seizure Psychogenic
EpidemiologyAnd clinical setting Female>malesYounger age (<55)Frequent episodes(>2)

Prolonged standing, extreme emotions, hot humid surrounding

 

Structural heart diseaseMales>femalesOlder age (>55 years)

Lesser episodes(<3)

In supine position or during exertion

Family history of sudden cardiac death

Younger age (<45yrs)Any clinical situation Females>malesOccurs in others presenceYoung age (<40 yrs)

Many episodes (many episodes in a day)

No definite trigger

 

Premonitory symptoms Longer duration(>5s)PalpitationsBlurred vision

Nausea

Warmth

Diaphoresis

Light-headedness

Shorter duration(<6s)Palpitation less common Sudden onsetBrief aura (déjà vu, olfactory, gustatory, visual Usually absent
During the episode Pallor & diaphoresisDilated pupilHypotension

Bradycardia

Urine and fecal incontinence

Brief clonic movements may occur

 

Cyanosed not paleIncontinenceClonic movements may occur Cyanosed, no pallorTongue bitingFrothing at mouth

Prolonged syncope(>5 mins)

Hypertension

Tachycardia

Horizontal eye deviations

Tonic-clonic movements

Normal colourNormal pulse and BPProlonged duration

No incontinence

Eyes closed

Residual symptoms CommonFatigueOriented Residual symptoms uncommon (unless prolonged unconsciousness) CommonMuscle achesDisorientation

Fatigue

Headache

Slow recovery

uncommon

 

Salient features of syncope due to less common causes

Cause of syncope Salient features
  1. Vascular steal syndromes (subclavian steal syndrome)

 

 

Syncope in association with symptoms of brain stem ischemia (i.e.,diplopia,tinnitus,focal weakness or sensory loss, vertigo, dysarthria.
  1. Migraine associated syncope
Throbbing unilateral headache, scintillating scotomata, nausea, vomiting, photophobia, phonophobia
  1. Orthostatic hypotension
History of orthostatic symptoms and syncope, features of autonomic failure and other neurological symptoms (e.g.,parkinsonism, disturbances of bowel, bladder , thermoregulatory and sexual function, ataxia)-volume depletion-drug and alcohol induced
  1. Carotid sinus hypersensitivity
Common in elderly, relationship to specific neck positions (neck collar, shaving etc.), carotid sinus massage reproduces symptoms or bradycardia
  1. Situational syncope
Related to specific situations ( cough, defecation, laugh, swallow, after food, sneeze, micturition etc.)
  1. Glossopharyngeal syncope
Associated with glossopharyngeal neuralgia

 

These tables provide enough information to help in diagnosis. Clinical history and physical examination has around 25% sensitivity for etiologic diagnosis of syncope. Most of these patients need further evaluation.

Special note for students about to appear in exams:
Remember the structural heart diseases which result in syncope. Important ones
1. LVOTO- aortic stenosis, HCM, coarctation of aorta
2. RVOTO – pulmonary stenosis
3. Pulmonary hypertension
4. Atrial myxoma
These conditions will have a lot of other cardiac symptoms which will help in making a clinical diagnosis. You will have to remember the natural history of important structural heart diseases and exam cases.

This article is part of the series about history taking in cardiology and is intended primarily for medical students. Physicians and practitioners are referred to ESC guideline on evaluation and management of syncope (http://www.escardio.org/guidelines-surveys/esc-guidelines/guidelinesdocuments/guidelines-syncope-ft.pdf).

Keywords : history taking in cardiology, medical students, syncope, symptoms of heart disease, analysis of symptoms

APPROACH TO PALPITATION

APPROACH TO PALPITATION

History taking in cardiology contd…

Palpitation is a common symptom in cardiac patients as well as in patients with a variety of other diseases, sometimes even without diseases. History taking represents a major part of evaluation of patients with palpitation as most patients by the time they visit a physician have no palpitation and the diagnosis has to be made retrospectively.

Before embarking on the understanding of palpitation we should know what palpitation is. As defined by EHRA (European heart rhythm association) “Palpitations are a symptom defined as awareness of the heartbeat and are described by patients as a disagreeable sensation of pulsation or movement in the chest and/or adjacent areas.”

Even though palpitation is a very common symptom it is a difficult problem to evaluate and to make a definitive diagnosis.

Below is given a list of the possible etiologies of palpitation. Take a careful look into the list  so that you understand what we are looking for while taking history of palpitation.

Etiologies of palpitation:

  1. Cardiac arrhythmias

Supraventricular/ventricular extrasystoles

Supraventricular/ventricular tachycardias

Bradyarrhythmias: severe sinus bradycardia, sinus pauses, second and

third-degree atrioventricular block

Anomalies in the functioning and/or programming of pacemakers and ICDs

  1. Structural heart diseases

Mitral valve prolapse

Severe mitral regurgitation

Severe aortic regurgitation

Congenital heart diseases with significant shunt

Cardiomegaly and/or heart failure of various aetiologies

Hypertrophic cardiomyopathy

Mechanical prosthetic valves

  1. Psychosomatic disorders

Anxiety, panic attacks

Depression, somatization disorders

  1. Systemic causes

Hyperthyroidism, hypoglycaemia, postmenopausal syndrome, fever,

anaemia, pregnancy, hypovolaemia, orthostatic hypotension,

postural orthostatic tachycardia syndrome, pheochromocytoma,

arteriovenous fistula

  1. Effects of medical and recreational drugs

Sympathicomimetic agents in pump inhalers, vasodilators,

anticholinergics, hydralazine

Recent withdrawal of b-blockers

Alcohol, cocaine, heroin, amphetamines, caffeine, nicotine, cannabis,

synthetic drugs

Weight reductions drugs

Now lets go to the history taking proper. Here we will have our standard step-wise approach to history taking and analysis (as mentioned in approach to chest pain)

Step 1: describe the symptom in detail

Step2: localize the symptom to an anatomical system

Step 3: localize the palpitation to an organ/mechanism

Step 4: etiology of palpitation

As described in history taking in cardiology , always begin by noting down the premorbid functional status of the patient. Any change in functional status should be noted.

Step 1.Recording the history of palpitation:

Given here is a scheme of question to ask while taking history of palpitation

  1. Circumstances prior to the beginning of palpitations

Activity (rest, sleeping, during sport or normal exercise, change in

posture, after exercise)

Position (supine or standing)

Predisposing factors (emotional stress, exercise, squatting or

bending)

  1. Onset of palpitations

Abrupt or slowly arising

Preceded by other symptoms (chest pain, dyspnoea, vertigo, fatigue,

etc.)

  1. Episode of palpitations

Type of palpitations (regular or not, rapid or not, permanent or not)

Associated symptoms (chest pain, syncope or near syncope,

sweating, pulmonary oedema, anxiety, nausea, vomiting, etc.)

  1. End of the episode

Abrupt or slowly decreasing, end or perpetuation of accompanying

symptoms, duration, urination

Spontaneously or with vagal manoeuvres or drug administration

  1. Background

Age at the first episode, number of previous episodes, frequency

during the last year or month

Previous cardiac disease

Previous psychosomatic disorders

Previous systemic diseases

Previous thyroid dysfunction

Family history of cardiac disease, tachycardia or sudden cardiac

death

Medications at the time of palpitations

Drug abuse (alcohol and/or others)

Electrolytes imbalance

Step 2:

Once the history of palpitation has been recorded, next step is to localize whether it is cardiac or noncardiac in origin (please refer to the Etiology list for cardiac and noncardiac causes). It may be less reliable to differentiate a cardiac from noncardiac cause of palpitation based on history only. For that associated symptoms really help. Someone who has other symptoms of cardiac disease has more likelihood of having cardiac cause of palpitation.

Step 3:

Among cardiac cause of palpitation our aim is to differentiate arrhythmic from nonarrhythmic causes.

Features which suggest arrhythmic palpitations are

Structural heart disease

Primary electrical heart disease

Abnormal ECG

Family history of sudden death

Advanced age

Tachycardiac palpitations

Palpitations associated with haemodynamic impairment

Below are listed description of some common types of palpitation.

Type ofpalpitation  Subjectivedescription  Heartbeat Onset andtermination  Triggersituations  Possible associated symptoms
Extrasystolic ‘Skipping/missing a beat’, ‘sinking of the heart’ Irregular, interspersed withperiods of normal heartbeat  Sudden Rest
Tachycardiac ‘Beatingwings’ in the chest Regular or irregular, markedly accelerated Sudden Physical effort, cooling down Syncope,dyspnoea,fatigue,chestpain
Anxiety-related Anxiety, agitation Regular,slightly accelerated Gradual Stress,Anxiety attacks

 

Tingling in the hands and face, lump in the throat,atypical chest pain,sighing dyspnoea 
Pulsation Heart pounding Regular,normal frequency Gradual Physicaleffort Asthenia

 

Some features also help to differentiate the different types of arrhythmic palpitations:

Type of arrhythmia Heartbeat Trigger situation Associated symptoms Vagal manoeuvres
AVRT, AVNRT Sudden onset regular with periods of elevated heart rate Physical effort, changes in posture Polyuria, frog sign Sudden interruption
Atrial fibrillation Irregular with variable heart rate Physical effort, cooling down,post meal, alcohol intake Polyuria Transitory reduction in heart rate
Atrial tachycardia and atrial flutter Regular (irregular if A-V conduction is variable) with elevated heart rate Transitory reduction in heart rate
Ventricular tachycardia Regular with elevated heart rate Physical effort Signs/symptoms of hemodynamic impairment No effect

 

These tables will help to delineate the cardiac cause of palpitation.

 

Step 4:

This the final step where all the above discussion culminates in a list of differential diagnosis. The differential diagnosis will look something like this

  1. Arrhythmic palpitation
  2. Structural heart disease e.g.
    1. Valvular regurgitation
    2. Congenital or acquired shunt lesions
  3. Heart failure    etc..

 

In the exams it is a bit difficult to make  differential diagnoses based on palpitation only. There evaluate other cardiac symptoms very carefully. Once all the cardiac symptoms have been analysed then forming differential diagnoses is a bit easy. Yes one more thing read the natural history of cardiac diseases. I will post articles on natural history of cardiac diseases once this discussion on history taking is over.

This outlines the approach to palpitation. I hope it fulfils your purpose. All these articles are intended for medical students and exam goings. For professional there are a few references listed below for further reading.

Further readings:

  1. Weber BE, Kapoor WH. Evaluations and outcomes of patients with palpitations.

Am J Med 1996;100:138–48.

  1. Thavendiranathan P, Bagai A, Khoo C, Dorian P, Choudhry NK. Does this patient

with palpitations have a cardiac arrhythmia? JAMA 2009;302:2135–43.

  1. Hoefman E, Boer KR, van Weert HCPM, Reitsma JN, Koster RW, Bindels PJE.

Predictive value of history taking and physical examination in diagnosing arrhythmias

in general practice. Fam Pract 2007;24:636–41.

  1. Managing patients with palpitation. Europace (2011) 13, 920–934

Approach to chest pain

History taking in cardiology cont..

Chest pain is a common symptom of a variety of diseases. Developing a clear and thorough approach to chest pain is immensely important for your day to day practice and also for students for their assessments and exams. The spectrum of diseases producing chest pain range from innocuous conditions like muscle aches to life threatening myocardial infarction and aortic dissection.

Developing an approach to chest pain:

I will discuss in detail the approach which will be applicable for case presentation in exams and also for day to day practice.

The approach to chest pain can be divided into four steps

Step-1: this should include a thorough description of the symptom. Characterize the pain in the best possible detail

Step-2: localization of the pain to the different anatomic systems in the chest like – respiratory system, cardiovascular system, musculoskeletal system, gastrointestinal tract, hepato-pancreato-biliary system, neurological system.

Step-3: since we are mainly concerned with the cardiovascular system, the next step is localization of the chest pain to different cardiac structures – pericardium, coronary arteries, myocardium, endocardial structures and aorta.

Step-4: And finally etiology of chest pain.

A thorough understanding of each step is of paramount importance. At the end of history you should be able to form a list of etiologic differential diagnoses ranked according to priority.

Does this sound too much? Its not actually as you will discover as you read further.

Step-1: describing the chest pain

Describe the chest pain in the following headings

  1. Quality of pain – the common terms used to describe different types of chest pain are deep, boring, chest discomfort, tightness, heaviness, uneasiness, pricking, choking, sharp, shooting, ripping pain etc
  2. Location of pain- try to elicit the exact location by asking the patient to point to point to the site of maximum pain
  3. Radiation of pain
  4. Onset of pain- acute onset or insidious onset
  5. Tempo of progression
  6. Duration of symptoms
  7. Aggravating factors
  8. Relieving factors
  9. Positional variation in pain
  10. Any associated symptoms
    1. Other cardiac symptoms – shortness of breath, palpitation, fatigue, syncope, dizziness, cyanosis
    2. Respiratory symptoms- cough, expectoration, wheezing, hemoptysis, shortness of breath etc
    3. Gastrointestinal symptoms- nausea, vomiting, relation to food, dysphagia, odynophagia,
    4. Any neurological symptoms
    5. Any pain, redness or swelling at site of pain

Once this characterization part is over move to step-2

Step-2: Localization of pain to different organ systems:

The key to localization of the symptom to a particular system is the above characterization of pain. Below is a table of the salient features of each system.

SYSTEM SYNDROME CLINICAL DESCRIPTION KEY DISTINGUISHING FEATURES
Cardiac Angina Retrosternal chest pressure, burning, or heaviness; radiating occasionally to neck, jaw, epigastrium, shoulders, left arm Precipitated by exercise, cold weather, or emotional stress; duration 2-10 min, relieved by rest or nitrates
Rest or unstable angina Same as angina, but may be more severe Typically <20 min; lower tolerance for exertion; crescendo pattern
Acute myocardial infarction Same as angina, but may be more severe Sudden onset, usually lasting ≥30 min; often associated with shortness of breath, weakness, nausea, vomiting
Pericarditis Sharp, pleuritic pain aggravated by changes in position; highly variable duration Pericardial friction rub
Vascular Aortic dissection Excruciating, ripping pain of sudden onset in anterior of chest, often radiating to back Marked severity of unrelenting pain; usually occurs in setting of hypertension or underlying connective tissue disorder such as Marfan syndrome
Pulmonary embolism Sudden onset of dyspnea and pain, usually pleuritic with pulmonary infarction Dyspnea, tachypnea, tachycardia, signs of right heart failure
Pulmonary hypertension Substernal chest pressure, exacerbated by exertion Pain associated with dyspnea and signs of pulmonary hypertension
Pulmonary Pleuritis and/or pneumonia Pleuritic pain, usually brief, over involved area Pain pleuritic and lateral to midline, associated with dyspnea
Tracheobronchitis Burning discomfort in midline Midline location, associated with coughing
Spontaneous pneumothorax Sudden onset of unilateral pleuritic pain, with dyspnea Abrupt onset of dyspnea and pain
Gastrointestinal Esophageal reflux Burning substernal and epigastric discomfort, 10-60 min in duration Aggravated by large meal and postprandial recumbency; relieved by antacid
Peptic ulcer Prolonged epigastric or substernal burning Relieved by antacid or food
Gallbladder disease Prolonged epigastric or right upper quadrant pain Unprovoked or following meal
Pancreatitis Prolonged, intense epigastric and substernal pain Risk factors including alcohol, hypertriglyceridemia, medications
Musculoskeletal Costochondritis Sudden onset of intense fleeting pain May be reproduced by pressure over affected joint; occasionally, swelling and inflammation over costochondral joint
Cervical disc disease Sudden onset of fleeting pain May be reproduced with movement of neck
Trauma or strain Constant pain Reproduced by palpation or movement of chest wall or arms
Infectious Herpes zoster Prolonged burning pain in dermatomal distribution Vesicular rash, dermatomal distribution
Psychological Panic disorder Chest tightness or aching, often accompanied by dyspnea and lasting 30 minutes or more, unrelated to exertion or movement Patient may have other evidence of emotional disorder

 

This table provides a lot of information. Once you go through the table a list of differential diagnoses can be made and appropriate investigations ordered.

The next discussion is for case presentation in exams

Step-3: the above table also helps in localizing the cardiovascular structures causing the pain.

Step-4: Etiology of cardiovascular cause of chest pain:

Finally you have to think of the Etiology of the cardiac chest pain. Now we will examine the common etiologies of chest pain and try to differentiate them clinically.

  1. Coronary artery disease: there will be history of angina as described in the table
  2. Left ventricular outflow tract obstruction (LVOTO): the symptoms of LVOTO are remembered by the letters – ASD- Angina, Syncope and Dyspnea. RVOTO also has similar symptoms. They may have additional features of right heart failure like- peripheral edema, ascites, right upper quadrant pain, neck pulsations, cyanosis etc
  3. Mitral stenosis and less commonly mitral regurgitation can have chest pain. But the predominate symptoms in case of
    1. Mitral stenosis: dyspnea
    2. Mitral regurgitation: fatigue and palpitation
  4. Pulmonary arterial hypertension: can have angina. The predominant symptoms will be dyspnea, fatigue. Associated symptoms can be palpitation, syncope.

This will cover some of the common cardiac causes of chest pain for exam case presentation.

Conclusion: Chest pain is a common symptom with a wide spectrum of presentation. Attention to the details of history will help to narrow down the possible conditions giving rise to the chest pain.

Your comments, suggestions and corrections are most welcome and will greatly help me to improve my articles.

Thank you

Dr. Anupam Jena
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