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About Anupam

Interventional Cardiologist and Electrophysiologist

Asia Pacific Heart Rhythm Society (APHRS 2016)


I had this great opportunity to attend the 9th Asia Pacific Heart Rhythm Society Annual Conference 2016, at Seoul, South Korea. It was a great experience to listen to renowned authorities in the field of Cardiac Electrophysiology.

It was attended by around 3000 delegates from around the world.

That’s my mentor, Prof. Young-Hoon Kim. A great electrophysiologist and human being also the principal force behind the successful organization of APHRS.

I had the opportunity to participate in a session on Difficult Transseptal Punctures.

That’s me

The best part for me was that I got a Young Investigator award for our study on repeat VT ablations

 Wow, that was an experience to remember.

Finally, there was a live case of AF ablation from our center.

The conference concluded on 15th October 2016, but the lasting impression will remain with me for a long time.

DR. ANUPAM JENA
INTERVENTIONAL CARDIOLOGIST & ELECTROPHYSIOLOGIST
KALINGA INSTITUTE OF MEDICAL SCIENCES
BHUBANESWAR, ODISHA
INDIA
EMAIL: drjena@live.com

Ventricular Tachycardia – Classification

Ventricular Tachycardia – Classification

Ventricular tachycardia is a common arrhythmia. The manifestations include mild symptoms of palpitation to sudden death. In next few blog posts, we will try to understand the basics of ventricular tachycardia/fibrillation and we will discuss management of these arrhythmias.

Definition:

Ventricular arrhythmias are defined as arrhythmias that originate below the bifurcation of His bundle, in the specialized conduction system, the ventricular muscle, or in combination of both tissues.

electrocardiogram_of_ventricular_tachycardia

Ventricular Tachycardia ECG

(Image created by Karthik Sheka, M.D. [CC BY-SA 2.5 (http://creativecommons.org/licenses/by-sa/2.5)], via Wikimedia Commons)

There are different classifications of ventricular arrhythmias, according to their duration, morphology of QRS complexes, and clinical characteristics.

Classification According to Duration

(1) Premature ventricular complexes (PVC): isolated complexes originating from the His-Purkinje system or ventricular myocardium.
(2) VT: 3 or more consecutive QRS complexes at a rate greater than 100 beats per minute.
(3) Nonsustained VT: VT that terminates spontaneously within 30 seconds.
(4) Sustained VT: continuous VT lasting for ≥30 seconds or that requires an intervention for termination (such as cardioversion).

Classification According to Morphology of QRS Complexes

(1) Monomorphic VT: VT that has a similar QRS configuration from beat to beat. Some variability in QRS morphology at initiation is not uncommon.
(2) Multiple monomorphic VT: more than one morphologically distinct monomorphic VT, occurring as different episodes or induced at different times.
(3) Polymorphic VT: VT that has a continuously changing QRS configuration indicating a changing ventricular activation sequence.
(4) Pleomorphic VT: VT that has more than one morphologically distinct QRS complex occurring during the same episode of VT, but the QRS is not continuously changing.
(5) Ventricular flutter: rapid VT that has a sinusoidal QRS configuration that prevents identification of the QRS morphology.
(6) VF: ventricular tachyarrhythmia that has a totally chaotic
morphology.

Classification According to Clinical Characteristics

(1) Clinical VT: VT that has occurred spontaneously based on analysis of 12-lead ECG QRS morphology and rate.
(2) Hemodynamically unstable VT: VT that causes hemodynamic compromise requiring prompt termination.
(3) Incessant VT: continuous sustained VT that recurs immediately despite repeated spontaneous or therapeutic termination.
(4) Repetitive monomorphic VT: continuously repeating episodes of self-terminating nonsustained VT.
(5) VT storm: 3 or more separate episodes of sustained VT within 24 hours, each requiring termination by an intervention.
(6) Unmappable VT: VT that does not allow interrogation of multiple sites to define the activation sequence or perform entrainment mapping. It may be due to hemodynamic
intolerance that necessitates immediate VT termination, spontaneous, or pacing-induced transition to other morphologies of VT, or repeated termination during mapping.

In the next post, we will discuss clinical features and ECG features.

DR. ANUPAM JENA
CONSULTANT INTERVENTIONAL CARDIOLOGIST & ELECTROPHYSIOLOGIST
KALINGA INSTITUTE OF MEDICAL SCIENCES
BHUBANESWAR, ODISHA
INDIA
EMAIL: drjena@live.com

Primary prevention ICD in Nonischemic cardiomyopathy

There is a recent online first article in NEJM  ( Defibrillator Implantation in Patients with Nonischemic Systolic Heart Failure – DANISH Study). The study is summarized below:

Summary:

The benefit of an implantable cardioverter–defibrillator (ICD) in patients with symptomatic systolic heart failure caused by coronary artery disease has been well documented. However, the evidence for a benefit of prophylactic ICDs in patients with systolic heart failure that is not due to coronary artery disease has been based primarily on subgroup analyses. The management of heart failure has improved since the landmark ICD trials, and many patients now receive cardiac resynchronization therapy (CRT).

Methods

In a randomized, controlled trial, 556 patients with symptomatic systolic heart failure (left ventricular ejection fraction, ≤35%) not caused by coronary artery disease were assigned to receive an ICD, and 560 patients were assigned to receive usual clinical care (control group). In both groups, 58% of the patients received CRT. The primary outcome of the trial was death from any cause. The secondary outcomes were sudden cardiac death and cardiovascular death.

Results

After a median follow-up period of 67.6 months, the primary outcome had occurred in 120 patients (21.6%) in the ICD group and in 131 patients (23.4%) in the control group (hazard ratio, 0.87; 95% confidence interval [CI], 0.68 to 1.12; P=0.28). Sudden cardiac death occurred in 24 patients (4.3%) in the ICD group and in 46 patients (8.2%) in the control group (hazard ratio, 0.50; 95% CI, 0.31 to 0.82; P=0.005). Device infection occurred in 27 patients (4.9%) in the ICD group and in 20 patients (3.6%) in the control group (P=0.29).

Conclusions

In this trial, prophylactic ICD implantation in patients with symptomatic systolic heart failure not caused by coronary artery disease was not associated with a significantly lower long-term rate of death from any cause than was usual clinical care.

This is the summary of the study. This study proves the point that primary prevention ICD doesn’t reduce the all cause mortality. But there are few points to consider in this very well designed study:

  1. SCD was the cause of death in 24 out of 120 (20%) total deaths in the ICD group. SCD was the cause of death in 46 out of 131 (35%) total deaths in the non-ICD (usual care group). So that means majority of mortality even in the non-ICD usual care group are due to non arrhythmic causes.
  2. The number of non-arrhythmic mortality in the ICD group is 96 out of total of 120 (80%) and in the non-ICD group is 65%.
  3. The question still remains that – How is a device (i.e. ICD) which prevents arrhythmic deaths, is expected to reduce the All Cause Mortality (the primary end point of this study) when the majority of deaths are due to non-arrhythmic causes.
  4. When considering the sudden cardiac deaths, ICD definitely reduced the mortality [Sudden cardiac death occurred in 24 patients (4.3%) in the ICD group and in 46 patients (8.2%) in the control group (hazard ratio, 0.50; 95% CI, 0.31 to 0.82; P=0.005)].

This study is a landmark study. It shows that the present indications for primary prevention ICD in non-ischemic cardiomyopathy are likely  include patients who may not after all benefit from a primary prevention ICD. It further shows that ICD is effective in preventing SCD in non-ischemic cardiomyopathy.

So to conclude this important study shows that we need to find markers of SCD in non-ischemic cardiomyopathy so that ICD implantation can be more effectively done in patients who are at high risk of SCD.

(Disclaimer: The views expressed are entirely personal of the author of this blog and are aimed towards an educational discussion on the study. These opinions are not meant for application in medical practice and are for the purpose of discussion only)

Keywords: Electrophysiology, Cardiomyopathy, Implantable cardioverter defibrillator, Sudden cardiac death

Arrhythmia or Disorders of Heart Rhythm

Arrhythmias or disorders of heart rhythm are a group of diseases characterized by abnormality of heart beat. Our heart is expected to beat in a certain way. In an adult individual the heart normally beats 60 t0 100 times per minute, in a regular manner (that means a nearly constant interval between two beats ). There are some normal variations, like in children the heart beat is faster, in some healthy persons and trained athelets the heart beat can be slower, during sleep the heart beat is normally slower.

Definition of Arrhythmia:

Arrhythmia is defined as any deviation from this normal pattern of heart beat.

What are the types of Arrhythmia?

Heart rhythm disorders are basically of two types. When the Heart rate is abnormally high it is called TACHYCARDIA. When the heart rate is abnormally slow it is called BRADYCARDIA. There can be irregular heart beats even if the heart rate is between 60-100, those cases are also Arrhythmic.

What is the relation of arrhythmias to other heart diseases?

Arrhythmias can be divided into two types based on heart diseases

  1. Arrhythmias occurring in persons having no underlying structural heart disease are called- IDIOPATHIC ARRHYTHIMAS
  2. Arrhythmia also arise in persons who have underlying structural heart diseases.

What are the symptoms of Arrhythmia?

Arrhythmias due to slow heart rate (Bradycardia) commonly cause

  1. Lethargy
  2. Fatigue
  3. Palpitation
  4. Light headedness
  5. Syncope (Transient loss of consciousness followed by full recovery)
  6. Sudden death

Arrhythmias due to fast heart rate (Tachycardia) commonly produce symptoms of

  1. Palpitation
  2. Faintness and light headedness
  3. Syncope (Transient loss of consciousness followed by full recovery)
  4. Sudden death
  5. Reduced pumping capacity of heart and related symptoms
  6. Some arrhythmias like atrial fibrillation can produce abnormal clotting of blood inside heart which can migrate to brain to cause stroke and paralysis.

How serious are Arrhythmias?

Some arrhythmias are benign and non life threatening, but they cause troublesome symptoms of palpitation and skipped beats.

Some arrhythmias are life threatening and can cause even sudden death. It all depends on the origin and type of arrhythmias and any other underlying heart disease.

How to diagnose arrhythmia?

Arrhythmias are commonly diagnosed by

  • ECG
  • Holter monitoring
  • Sometimes long term monitoring like – event recorders, loop recorders etc.
  • In some case Cardiac Electrophysiological study is required to diagnose a rhythm disorder.

What are the treatments available?

  1. Some transient arrhythmias terminate on their own and don’t need any specific therapy
  2. Underlying cause needs to be treated like- drugs, electrolyte disturbances, etc
  3. Medicines are usually the first line treatment
  4. Catheter Ablation: It is a procedure done in cardiac cathlab where an arrhythmia is ablated commonly by application of radiofrequency energy inside the heart. It is a safe procedure with prospect for complete cure of the arrhythmia.

 

DR. ANUPAM JENA
CONSULTANT INTERVENTIONAL CARDIOLOGIST & ELECTROPHYSIOLOGIST
KALINGA INSTITUTE OF MEDICAL SCIENCES
BHUBANESWAR, ODISHA
INDIA
EMAIL: drjena@live.com

 

 

 

 

 

Cardiology MCQ – 14.05.2016


What is the most probable site of origin of the tachycardia in a patient with structurally normal heart ?

MA VT epicardial1. Right ventricular outflow tract

2. Mitral annular VT

3. Tricuspid annulus

4. Idiopathic left fascicular VT

Atrial septal defect and Pregnancy – Patient Information

What is atrial septal defect (ASD)

Atrial Septal defect is an abnormal communication between the upper two chambers of the heart namely left atrium and right atrium. Normally the left and right atrium are separated by the interatrial septum. So in atrial septal defect (ASD)  a part of the interatrial septum is missing. See the image below

Atrial Septal Defect

(Source : www.wikipedia.org)

In patients with ASD there is mixing of oxygenated blood of left side with venous blood on the right side.

Pregnancy Issues:

Patients with even a large unrepaired secundum atrial septal defect usually tolerate pregnancy without complications. In cases where the ASD has been closed either by surgery or by device, the course of pregnancy is similar to a normal female without heart disease, except when there are preexisting problems with heart rhythm or pulmonary hypertension.

Complications:

The complications include

1- Disorders of heart rhythm – e.g. Atrial fibrillation

2. Pulmonary hypertension – where there is increased pressure in the blood vessels of the lung.

3. Paradoxical embolism – Sometimes blood clots formed in the leg veins (increased chances in pregnant females) can pass through the defect in the heart and get lodged in the brain and can cause stroke .

Precautions:
  1. Elective closure of ASD before contemplating pregnancy is advisable
  2. Meticulous attention should be paid to the maternal leg veins, particularly during peridelivery, because deep venous thrombosis could precipitate a paradoxical embolus and stroke.
  3. In case of any complication like atrial fibrillation, pulmonary hypertension, close follow-up with a cardiologist is recommended.
Keywords: Congenital heart disease, pregnancy and heart disease, Patient information, atrial septal defect.

Myocardial Infarction- Third Universal definition and classification

Definition of myocardial infarction

Criteria for acute myocardial infarction :

The term acute myocardial infarction (MI) should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischaemia. Under these conditions any one of the following criteria meets the diagnosis for MI:

Detection of a rise and/or fall of cardiac biomarker values [preferably cardiac troponin (cTn)] with at least one value above the 99th percentile upper reference limit (URL) and with at least one of the following:

  1. Symptoms of ischaemia.
  2. New or presumed new significant ST-segment–T wave (ST–T) changes or new left bundle branch block (LBBB).
  3. Development of pathological Q waves in the ECG.
  4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.
  5. Identification of an intracoronary thrombus by angiography or autopsy.

•Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurred before cardiac biomarkers were obtained,or before cardiac biomarker values would be increased.

• Percutaneous coronary intervention (PCI) related MI is arbitrarily defined by elevation of cTn values (>5 x 99th percentile URL) in patients with normal baseline values (≤99th percentileURL) or a rise of cTnvalues >20% if the baseline values are elevated and are stable or falling. Inaddition,either(i)symptoms suggestiveof myocardialischaemia or (ii) new ischaemic ECG changes or (iii) angiographicfindings consistent with a proceduralcomplication or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required.

• Stent thrombosis associated with MI when detected by coronary angiography or autopsy in the setting of myocardial ischaemia and with a rise and/or fall of cardiac biomarker values with at least one value above the 99th percentile URL.

• Coronary artery bypass grafting (CABG) related MI is arbitrarily defined by elevation of cardiac biomarker values (>10 x 99th percentile URL) in patients with normal baseline cTn values (≤99th percentile URL). In addition, either (i) new pathological Q waves or new LBBB,or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.

Criteria for prior myocardial infarction

Any one of the following criteria meets the diagnosis for prior MI:

• Pathological Q waves with or without symptoms in the absence of non-ischaemic causes. • Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract,in the absence of a non-ischaemic cause.

• Pathological findings of a prior MI

 UNIVERSAL CLASSIFICATION OF MYOCARDIAL INFARCTION

Type 1: Spontaneous myocardial infarction

Spontaneous myocardial infarction related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have underlying severe CAD but on occasion non-obstructive or no CAD.

Type 2: Myocardial infarction secondary to an ischaemic imbalance

In instances of myocardial injury with necrosis where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand, e.g.coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy-/brady-arrhythmias, anaemia, respiratory failure, hypotension, and hypertension with or without LVH.

Type 3: Myocardial infarction resulting in death when biomarker values are unavailable

Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurring before blood samples could be obtained, before cardiac biomarker could rise, or in rare cases cardiac biomarkers were not collected.

Type 4a: Myocardial infarction related to percutaneous coronary intervention (PCI)

Myocardial infarction associated with PCI is arbitrarily defined by elevation of cTn values >5 x 99th percentile URL in patients with normal baseline values (£99th percentile URL) or a rise of cTn values >20% if the baseline values are elevated and are stable or falling. In addition, either (i) symptoms suggestive of myocardial chaemia, or (ii) new ischaemic ECG changes or new LBBB, or (iii) angiographic loss of patency of a major coronary artery or a side branch or persistent slow- or no-flow or embolization, or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required.

Type 4b: Myocardial infarction related to stent thrombosis

Myocardial infarction associated with stent thrombosis is detected by coronary angiography or autopsy in the setting of myocardial ischaemia and with a rise and/ or fall of cardiac biomarkers values with at least one value above the 99th percentile URL.

Type 5: Myocardial infarction related to coronary artery bypass grafting (CABG)

Myocardial infarction associated with CABG is arbitrarily defined by elevation of cardiac biomarker values >10 x 99th percentile URL in patients with normal baseline cTn values (£99th percentile URL).In addition,either (i) new pathological Q waves or new LBBB,  or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality

AMBITION: Initial Use of Ambrisentan plus Tadalafil in Pulmonary Arterial Hypertension

Data on the effect of initial combination therapy with ambrisentan and tadalafil on
long-term outcomes in patients with pulmonary arterial hypertension are scarce.

METHODS
In this event-driven, double-blind study, patients were randomly assigned, in a 2:1:1 ratio,
participants with World Health Organization functional class II or III symptoms of pulmonary arterial hypertension who had not previously received treatment to receive
initial combination therapy with 10 mg of ambrisentan plus 40 mg of tadalafil (combination-therapy group), 10 mg of ambrisentan plus placebo (ambrisentanmonotherapy group), or 40 mg of tadalafil plus placebo (tadalafil-monotherapy group), all administered once daily.

The primary end point in a time-to-event analysis was the first event of clinical failure, which was defined as the first occurrence of a composite of death, hospitalization for worsening pulmonary arterial hypertension, disease progression, or unsatisfactory long-term clinical response.

RESULTS
The primary analysis included 500 participants; 253 were assigned to the combination-
therapy group, 126 to the ambrisentan-monotherapy group, and 121 to the tadalafil-monotherapy group. A primary end-point event occurred in 18%, 34%, and 28% of the participants in these groups, respectively, and in 31% of the pooled monotherapy group (the two monotherapy groups combined). The hazard ratio for the primary end point in the combination-therapy group versus the pooled-monotherapy group was 0.50 (95% confidence interval [CI], 0.35 to 0.72; P<0.001). At week 24, the combination-therapy group had greater reductions from baseline in N-terminal pro–brain natriuretic peptide levels than did the pooled-monotherapy group (mean change, −67.2% vs. −50.4%; P<0.001), as well as a higher percentage of patients with a satisfactory clinical response (39% vs. 29%; odds ratio, 1.56 [95% CI, 1.05 to 2.32]; P = 0.03) and a greater improvement in the 6-minute walk distance (median change from baseline, 48.98 m vs. 23.80 m; P<0.001). The adverse events that occurred more frequently in the combination-therapy group than in either monotherapy group included peripheral edema, headache, nasal congestion, and anemia.

CONCLUSIONS
Among participants with pulmonary arterial hypertension who had not received
previous treatment, initial combination therapy with ambrisentan and tadalafil
resulted in a significantly lower risk of clinical-failure events than the risk with
ambrisentan or tadalafil monotherapy.

Source : http://www.nejm.org/doi/full/10.1056/NEJMoa1413687?query=featured_home

Approach to Arrhythmia part 1: Bradycardia

Approach to Arrhythmia part 1: Bradycardia

Bradycardia is defined as heart rate <60/min. To understand the cause of bradycardia we have to understand the structures involved in the production and conduction of cardiac impulse.

The normal cardiac structures involved in electrical activity of the heart are
1. SA node- It is the pacemaker of the heart, because it fires at the highest rate hence predominates over other pacemakers of the heart.
2.AV node – In normal hearts its function is to conduct impulses generated in the SA node to the ventricles through the Bundle of His and bundle branches.It can act as a slow pacemeker when the SA node is diseased
3. Bundle of His and bundle branches- Normally their function is conduction of cardiac impulses. They can act as a slow pacemeker when the proximal structures (SA node & AV node) are diseased.
4. Purkinje fibres
5. Ventricular myocardium- In complete heart block the ventricular myocardium produces escape rhythm at a slow rate of 20-40/min

Disease in any of the structures can lead to bradycardia.

The diagnosis is made from ECG in most of the cases.
Now we will discuss how to systematically analyze an ECG for diagnosing a bradycardia.

Step 1: Calculate the rate first. Bradycardia by definition heart rate <60/min
Step 2: Analysis of rhythm begins with search for P-wave. Normally P-waves are produced by SA node, so absence of P-waves indicate disease of SA node. Which is called as sick sinus syndrome
Step 3: Absent P-waves can be due to
1. Sick sinus syndrome with escape rhythm. (R-R intervals fixed)
2. Atrial fibrillation with slow ventricular rate. (R-R intervals variable)

Sick sinus syndrome: no visible P waves, fixed R-R intervals.

Sick sinus syndrome: no visible P waves, fixed R-R intervals.

 

Step 4: P-waves present
If P-waves are present look for P-P interval, PR-interval and relation between P and R waves.

Step 5: P-P interval variable
Nonconducted APCs
Step 6: P-P interval fixed
The next stepis evaluation of PR-interval and relation between P and R waves

Step 7: PR interval normal and fixed: Sinus bradycardia

Sinus bradycardia

Sinus bradycardia

PR interval prolonged but fixed and each QRS complex is preceeded by P wave: First degree AV block

1st degree AV block: Prolonged fixed PR interval

1st degree AV block: Prolonged fixed PR interval

(ECG courtesy of www.lifeinthefastlane.com)
PR interval lengthens then dropped beat and return with short PR interrval: Mobitz type 1 second degree AV block

Wenckebach block

Wenckebach block

(ECG courtesy of www.lifeinthefastlane.com)
PR interval fixed then dropped beat : Mobitz type 2 second degree AV block
No PR relationship : Third degee AV block

Complete heart block

Complete heart block

(ECG courtesy of www.lifeinthefastlane.com)

 

The flow chart below summarizes the whole approach

ECG  approach to bradycardia

ECG approach to bradycardia