Tag Archives: Student Section

One MCQ a day – 11.04.2015

Answer to the question on 10.04.2015

Answer: B

Accessory pathways are anomalous bypass tracts composed of working myocardial cells. Most APs insert along the mitral or tricuspid valve and are referred to as AV accessory pathways. Approximately 60% of APs insert along the mitral valve and are referred to as left free-wall pathways. About 25% insert along the septal aspect of the tricuspid or mitral valve and are classified as septal pathways. The remaining 15% are right freewall pathways.

Occasionally one may encounter APs that do not insert along the AV valves. Examples include atriofascicular, nodoventricular, nodofascicular, and atrionodal pathways.

Atriofascicular pathways connect the right atrium to the distal ramifications of the right bundle branch and are capable of only anterograde conduction.

Nodoventricular and nodofascicular pathways connect the AV node to the right ventricular myocardium and the specialized conduction system, respectively.

Atriofascicular and nodoventricular/nodofascicular connections are also notable for their decremental conduction properties.

Atrionodal pathways are rare and connect the right atrial myocardium to the AV node.

(Ref: Cardiac Electrophysiology: From Cell to Bedside: 6th edition, Page : 755)

 

MCQ 11.04.2015

Q. Localize the accessory pathway (AP) from the ECG

ANTEROSEPTAL AP

A. Left free wall AP

B. Posteroseptal AP

C. Right free wall AP

D. Anteroseptal AP

Please post your answers as comments.

Keywords: Cardiology, Multiple choice questions, medical students, Electrophysiology

ECG-full

Simplest approach to reading the ECG. Part-1

APPROACH TO READING THE ECG

ECG or EKG (the electrocardiogram) has retained its role as the first and foremost investigations for many cardiovascular diseases. ECG is absolutely mandatory for diagnosis of heart rhythm and for myocardial ischemia. It has a prominent role in the diagnosis and management planning of a variety of cardiac diseases starting from heart failure and cardiomyopathy to valvular diseases and pericardial diseases.

Health care professionals are expected to be familiar with ECG. But to make sense of the variously shaped lines we need a few basic steps. Is article is part of a series of articles on ECG.

There is a systematic approach to reading the ECG. Medical students should always try to make a written report of the ECG according to the heading as listed below. Try to report as many ECGs as you get, and try to remember the systematic approach to ECG reading.

Now lets start with our ECG reading.

1. Speed – Paper speed is conventionally 25 mm/sec. It is normally written at the bottom of the Ecg.

2. Calibration – Vertically, the ECG graph measures the height (amplitude) of a given wave or deflection, as 10 mm (10 small boxes) equals 1 mV with standard calibration. Always check the calibration otherwise a false diagnosis of chamber enlargement or hypertrophy will be made or missed.

3. Rate

4. Rhythm

5. Axis

6. Loop (mainly in congenital heart disease)

7. P-wave

8. PR- interval

9. QRS complex

10. ST- segment

11. T-waves

12. QT- interval

13. U- Wave

14. Any other abnormal waves (like:- osborn wave, epsilon wave etc)

These 14 points when remembered and applied in the analysis of ECG will give the diagnosis in almost all cases.

We will further delineate each point in simple and clear terms in the subsequent posts.

APPOSITION IV : Trial

STENTYS SELF APPOSITION SES:

It is a self-expandable sirolimus-eluting coronary stent system, similar in concept to other self-expanding systems.

Watch the video:

Stentys self-apposition SES

APPOSITION IV trial:

Patients – 152 patients presenting with STEMI.

Design: Patients were randomized to Stentys self-apposing SES (Stentys, Paris, France; n = 90)   vs Resolute zotarolimus-eluting stent (ZES; Medtronic, Santa Rosa, CA; n = 62). Each treatment arm was then randomized to either 4- or 9-month follow-up.

 -Results: On QCA, no differences were observed between the treatment arms just after the procedure for in-stent minimal and mean lumen diameter. In-stent mean lumen diameter was larger at both 4- and 9-month follow-up for Stentys compared with Resolute (3.39 ± 0.46 mm vs 3.13 ± 0.35 mm).

-OCT demonstrated that Stentys SES was associated with fewer malapposed struts (0.07 ± 0.26% vs 1.16 ± 1.59%) and more covered struts (94.32 ± 5.69% vs 89.09± 5.65%) than Resolute ZES at 4 months. Percentage of stents with all struts covered was also higher with Stentys compared to Resolute ZES (33.3% vs 3.8%).

-No differences in malapposition (P = .55) or coverage (P = .81) were seen between the treatment arms in the 9-month cohort.

-Clinical outcomes were low and well balanced between stent groups in terms of MACE (P = .46), TVF (P = .46), and target vessel MI (P = .39).

-Predilatation Needed.

-The device is larger in profile as compared to DES

 Conclusion: Stentys, a self-apposing sirolimus-eluting stent (SES), shows ‘excellent’ apposition over time—better than an existing balloon-expandable drug-eluting stent—in patients with ST-segment elevation myocardial infarction (STEMI). The newer device is associated with faster strut coverage.

Your comments and insight most welcome

 

Genetic mutation in Metabolic Syndrome

A Form of the Metabolic Syndrome Associated with Mutations in DYRK1B — NEJM.

 

A founder mutation was identified in DYRK1B, substituting cysteine for arginine at position 102 in the highly conserved kinase-like domain. The mutation precisely cosegregated with the clinical syndrome. Functional characterization of the disease gene revealed that nonmutant protein encoded by DYRK1B inhibits the SHH (sonic hedgehog) and Wnt signaling pathways and consequently enhances adipogenesis. Furthermore, DYRK1B promoted the expression of the key gluconeogenic enzyme glucose-6-phosphatase. The R102C allele showed gain-of-function activities by potentiating these effects. A second mutation, substituting proline for histidine 90, was found to cosegregate with a similar clinical syndrome in an ethnically distinct family.

Conclusions

These findings indicate a role for DYRK1B in adipogenesis and glucose homeostasis and associate its altered function with an inherited form of the metabolic syndrome.

Colchicine in Stable Chronic Heart Failure

Heart failure is associated with activation of inflammatory cascades. this trial examines the effects of usig colchicine in Hf.

American College of Cardiology Foundation | JACC: Heart Failure | Anti-Inflammatory Treatment With Colchicine in Stable Chronic Heart FailureA Prospective, Randomized Study.

Approach to Dyspnea

History taking in Cardiology Contd….

Continuing our discussion on history taking in cardiology today we will form an approach to dyspnoea.

What is Dyspnea?

A consensus statement of the American Thoracic Society defined dyspnea in the following way1:

“Dyspnea is a term used to characterize a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioural responses.”

The American Thoracic Society (ATS) statement on the mechanisms, assessment, and management of dyspnea, as well as other ATS guidelines, can be accessed through the ATS web site at www.thoracic.org/statements.

It is one of the most common presentations of a variety of disorders.

What are we looking for when evaluating dyspnea?

In the approach to any symptom we should have a clear understanding of what we are looking for. Among patients who present with undue dyspnoea we are looking for one of the following major conditions:

  1. Respiratory system disease
    1. Asthma
    2. COPD
    3. Interstitial lung disease
    4. Pulmonary hypertension
  2. Cardiac disease
    1. Valvular heart disease
    2. Myocardial dysfunction either systolic or diastolic
    3. Pulmonary hypertension
    4. Pericardial diseases – though they present with symptoms of biventricular dysfunction or predominant right sided heart failure.
  3. Obesity
  4. Anaemia
  5. Deconditioning

Though this list is not complete but for all practical purposes these are the major differential diagnosis.

How to take history of dyspnoea?

General approach to record cardiac history:

In the description of any cardiac symptom you should proceed in a particular order. First describe the baseline (premorbid) functional status of the patient e.g. something like – the patient was able to walk for 5 kms, play golf, do jogging etc. without any symptoms.

Once the baseline functional status is clearly described go for symptoms. Any symptom should be described as ODP i.e. O= onset, D= duration, P= progression.

Describing the history:

  1. Onset of symptoms
  2. Duration of symptoms
  3. Progression (in terms of NYHA class and time to progression). In cardiovascular history always try to quantify symptoms in terms of NYHA class. Because it is the most widely used and validated.
  4. Describe the dyspnea in patient’s language. Try to ascertain that the patient actually has dyspnea. Sometimes the patient may be having predominant fatigue. Some of the common patient expressions of  dyspnea are like-
    • My breathing is shallow.
    • I feel an urge to breathe more.
    • My chest is constricted.
    • My breathing requires effort.
    • I feel a hunger for more air.
    • I feel out of breath.
    • I cannot get enough air.
    • My breath does not go in all the way.
    • My chest feels tight.
    • My breathing requires work.
    • I feel that I am smothering/suffocating.
    • I feel that I cannot get a deep breath.
    • I feel that I am breathing more.
    • My breath does not go out all the way.
    • My breathing is heavy.
    • Other descriptions

The language of dyspnoea can give a clue to the diagnosis e.g.

    1. Chest tightness or constriction is described in  Bronchoconstriction, interstitial oedema (e.g. Asthma, Myocardial ischemia)
    2. Increased work or effort of breathing is the description in – Airways obstruction, neuromuscular disease, reduced chest wall or pulmonary compliance (COPD, moderate to severe asthma, myopathy, pulmonary fibrosis)
    3. Air hunger, need to breathe, urge to breathe is seen in – increased drive to breathe (HF, pulmonary embolism, moderate to severe asthma or COPD)
    4. Rapid, shallow breathing- reduced chest wall or pulmonary compliance       (Interstitial fibrosis)
    5. Suffocating, smothering- Alveolar oedema (Pulmonary oedema)
    6. Heavy breathing, breathing more- Inadequate oxygen delivery to the muscles- Deconditioning

So carefully listen to the language patients use to describe the symptoms.

5. Variation in dyspnea – positional, diurnal or seasonal variation
6. Associated cough. If cough is there – dry or productive
7. Any history of wheezing
8. Haemoptysis
9. Orthopnoea or PND,History of PND is suggestive of cardiac disease. So always carefully ask for PND
10. Finally mention the present functional status of the patient.
Go to the next symptom like chest pain, palpitation , fatigue etc……only after you finish describing dyspnea

Once you are finished with describing the symptom of dyspnoea, formulate a short summary of the symptom. I will give an example of a summary – “patient had dyspnea which was insidious in onset and progressed from NYHA II to III/IV in …..Years, it is associated with h/o orthopnoea/PND, presently he is NYHA III.”

I hope this discussion is useful to you. Any suggestion, comments or correction is most welcome.

Dr. Anupam Jena
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Reference:

1.         Parshall MB, Schwartzstein RM, Adams L, et al. An official American Thoracic Society statement: update on the mechanisms, assessment, and management of dyspnea. American journal of respiratory and critical care medicine 2012;185:435-52.

 

History taking in Cardiology

History taking in any branch of medicine is the single most important exercise. Most clinical books open with the idea of history taking. In the initial part of medical training students sometimes fail to understand the importance of history taking. But as we go higher in our training we understand the importance of history gradually.

Why a good history is important?

A good history gives the diagnosis, or a list of differential diagnosis in most of the cases. Then you can channelize your investigations in that direction. Another practical need is for facing your clinical assessments and exams. The more you learn of a subject the more you understand about the history. History taking is a difficult job for the beginner. The skill improves with your knowledge in a field of medicine. These posts on “history taking in cardiology” will be an honest attempt by me to discuss the beauty and depth of history taking in cardiology.

How to take history in cardiology?

It is always safer to follow the standard format of history taking.

Patient particulars:

  1. Name
  2. Age
  3. Sex
  4. Address
  5. Educational status of the patient
  6. Occupation
  7. History given by self or parents/relatives
  8. If history given by relatives what do you think of the reliability of information given

When presenting your case in exams make this part of presentation sound like well-articulated sentences, e.g. the patient mr./mrs x.. ,is  a 55… years old male/female. He/she is a resident of y.. he is educated upto … and he/she works as ….history has been given by self/relative.

Make your presentation in a calm and composed manner, don’t sound haphazard and disorganized.

Presenting Complains:

Write the presenting complains in the proper chronological order. All of you might be aware of the chronological order in which symptoms are written. Usually the longest duration symptoms are mentioned first, followed by the second and so on.

Then comes history of present illness (HOPI)

In HOPI you should try to be systematic and proceeding in a well-directed manner. Now is the time to elaborate your presenting complains. It’s like what you want to keep as your diagnosis and differential diagnosis you talk more about them.

Those points we will discuss subsequently.

Basically history of present illness is analysis of symptoms.

What are symptoms of cardiovascular disease?

The presenting symptoms of cardiovascular disorders are

  1. Dyspnoea
  2. Chest pain
  3. Palpitation
  4. Fatigue
  5. Presyncope/Syncope/dizziness
  6. Pedal edema
  7. Neck pulsations
  8. Cyanosis
  9. Murmur
  10. Chest bulging, stunted growth, cyanotic spell – in paediatric cases

We will discuss about these symptoms one by one and how to analyse them

Past history:

Past history should include information about relevant diseases and conditions like diabetes mellitus, hypertension, bronchial asthma, tuberculosis, and other past medical and surgical conditions. In Indian setup history of rheumatic fever and treatment for same like penicillin prophylaxis should be sought.

Family history (Socio-economic history):

Is very important for cardiovascular diseases.

Personal history:

It includes questions about diet, addictions and substance abuse, etc.

Treatment history:

Ask about all previous investigations, drugs taken, procedures done

Summary of the entire history

Analysis of history

Differential diagnosis from history

Then proceed to physical examination

I will describe each component of the above outline in my subsequent posts

So keep reading. Any feedback or suggestion is welcome

Thank you

DR. ANUPAM JENA
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