Xray chest showing thickened and calcified pericardium

Eggshell calcification of the heart in constrictive pericarditis

 Eggshell calcification of the heart in constrictive pericarditis

Rajesh Vijayvergiya, Ramalingam Vadivelu, Sachin Mahajan, Sandeep S Rana, Manphool Singhal

World J Cardiol 2015 September 26; 7(9): 579-582

43/M presented with dyspnoea on exertion NYHA class III since 6 months. No other positive history.

On Examination:

HR-100/min  BP- 100/64   JVP- elevated, 18 cm; prominent X and Y descent

CVS: S1 S2 normal, Pericardial knock +

CXR : Calcified pericardium seen. See image

Echo: Thick, calcified pericardium.   > 25%  respiratory variation of mitral inflow velocities . Significant LV diastolic dysfunction

 

 

 

 

 

 

 

 

post bt shunt seroma

Interesting image- Post BT shunt seroma- a rare complication

Indian Heart J. 2014 Mar-Apr;66(2):227-30.

Post Blalock-Taussig shunt mediastinal mass – a single shadow with two different destinies

Rohit MK1, Vadivelu R2, Khandelwal N3, Krishna S3.

One of the rare complications following BT shunt surgery is seroma formation. It usually is benign and  x ray chest will reveal a mediatinal mass (left upper). CT scan usually confirms the diagnosis. Usually managed conservatively.

Image description:

Axial contrast chest CT obtained in a helical mode. The sagittal oblique maximal intensity projection image shows a small hypodense lesion of fluid attenuation seen adjacent to the BT shunt. No calcification, enhancement, septae, air foci or solid component was seen. Features are consistent with a post operative seroma. Thin long arrow points BT shunt. Broader, short arrow points seroma

 

dilated aortic root

When to intervene in patients with bicuspid aortic valve and dilated aortic root or ascending aorta

Circulation – December 4, 2015

Surgery for Aortic Dilatation in Patients with Bicuspid Aortic Valves:

 A Statement of Clarification from the American College of Cardiology/ American Heart Association Task Force on Clinical Practice Guidelines

Intervention in Patients with BAV and Dilatation of the Aortic Root (Sinuses) or Ascending Aorta:

  1. Operative intervention to repair or replace the aortic root (sinuses) or replace the ascending aorta is indicated in asymptomatic patients with BAV if the diameter of the aortic root or ascending aorta is 5 cm or greater

 

  1. Operative intervention to repair or replace the aortic root (sinuses) or replace the ascending aorta is reasonable in asymptomatic patients with BAV if the diameter of the aortic root or ascending aorta is 0 cm or greater and an additional risk factor for dissection is present (eg, family history of aortic dissection or aortic growth rate ≥0.5 cm per year) or if the patient is at low surgical risk and the surgery is performed by an experienced aortic surgical team in a center with established expertise in these procedures

 

  1. Replacement of the ascending aorta is reasonable in patients with BAV undergoing AVR because of severe aortic stenosis or aortic regurgitation when the diameter of the ascending aorta is greater than 4.5 cm
Reversal of factor X a inhibition

New Drug : Andexanet Alfa- Reversal agent for Factor X a inhibitors

NEJM- Nov 2015 – ANNEXA-A and ANNEXA-R ClinicalTrials

As of now the major limiting factor with the use of novel anticoagulants is the absence of  reversal agents in case of bleeding complications.

To find a solution to this problem, a new drug has been recently tested in ANNEXA-A and ANNEXA-R trials. Andexanet alfa, a new drug designed to reverse factor X a inhibition.

In the trial, Andexanet alfa was given to apixaban and rivoraxaban administrated healthy volunteers. Within minutes of administration anti factor Xa activity was reduced by more than 90% without any toxic or serious thrombotic effects.

Approach to the management of Venous thromboembolism

Step 1 :Confirm PTE or DVT diagnosis

Step 2: Look for contraindications for full dose anticoagulation. If contraindications exist then insert IVC filter.

Step 3 : If no contraindication then look for impending venous gangrene (in case of DVT) or cardiopulmonary collapse (cardiogenic shock/ RV dysfunction in case of PTE). If yes then start thrombolysis

Thrombolysis for DVT:

Indications : Impending venous gangrene, symptom duration < 14 days and low risk of bleeding

Mode : a)Catheter directed thrombolysis (CDT) : Fluroscopy guided placement of multiside holed catheter (pigtail) into the thrombus segment and infusing alteplase for 1-3 days at a rate of 0.5 mg to 3 mg/hour (50 mg diluted in 50 ml of NS). CDT is superior to systemic anticoagulation alone because of reduced post thrombotic syndrome and reduced bleeding complications

b)Pharmacomechanical Catheter directed thrombolysis (PCDT)

PCDT uses either the “Power Pulse” or “isolated thrombolysis” techniques. Power Pulse employs the AngioJet rheolytic thrombectomy system (Bayer, Warrendale, PA) to deliver and disperse the thrombolytic agent by a powerful pulse-spray injection. After bathing the clot in the thrombolytic agent, the AngioJet catheter aspirates the softened thrombus fragments. Isolated thrombolysis uses the Trellis peripheral infusion system (Covidien, Mansfield, MA) to deliver the thrombolytic agent directly into the clot. The agent is then circulated within the clot by an oscillating wire.

Advantage of PCDT over CDT : Reduced dose and infusion duration of alteplase thereby reducing bleeding complications and better efficacy

Thrombolysis for PTE :

For PTE there is insufficient evidence to recommend thrombolysis via a pulmonary artery catheter rather than systemic thrombolysis

Systemic thrombolysis dose: Alteplase 100 mg (10 mg as iv bolus over 10 min f/b 90 mg in 100 ml of NS infused over 2 hours)

Step 4

If there is no evidence of impending gangrene or cardiopulmonary collapse then initiate systemic anticoagulation

Phases of anticoagulation treatment:

Initial phase0 to 10 days:

IV or SC unfractionated heparin/LMWH/Fondaparinux/Rivaroxaban/Apixaban

Long term phase- 10 days to 3 months

Vitamin K antagonist – warfarin/acitrom (target INR: 2-3.5)

Rivaroxaban/Apixaban/Edoxaban/Dabigatran/LMWH

Extended phase-3 months to indefinite 

Indictions for extended therapy- 1.unprovoked/recurrent VTE    2. Malignancy related VTE

Drugs :

Vitamin K antagonist – warfarin/acitrom (target INR: 2-3.5)

Rivaroxaban/Apixaban/Edoxaban/Dabigatran/LMWH

Newer agents : Rivaroxaban(15 mg bd)/Apixaban(10 mg bd)/Edoxaban/Dabigatran(110 or 150 mg bd)

Pros- No need for INR monitoring, non-inferior or slightly efficacious then warfarin/acitrom, lesser major bleeding rates

cons- costlier, lesser availability especially in developing countries and no specific reversal agents

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

 

Cardiology MCQ 18.5.15

Q. All of the following are effective in the management of reflex syncope except

A. Life style modifications like avoiding triggers

B. Physical counterpressure maneuvers

C. Beta blockers

D. Cardiac pacing in patients with cardioinhibitory reflex syncope

Explanation:

According to ESC guideline 2009, beta blockers are no longer recommended and have been given class III recommendation for the treatment of reflex syncope. The first step in the management of reflex syncope is life style modifications like – avoiding triggers such as crowded places, prolonged standing etc.

-Physical counterpressure maneuvers are emerging as nonpharmacologic treatments for
syncope. These maneuvers include tensing of crossed legs, handgrip and arm tensing, abdominal binders, and support stockings.

-Class IIa recommendations include cardiac pacing for patients with dominant cardioinhibitory, carotid sinus sensitivity, and frequently recurrent reflex syncope after 40 years of age with documented cardioinhibitory responses during monitoring.

-Remember that pacemaker implantation in patients with reflex syncope and no evidence of cardioinhibitory reflexes is not indicated and can be harmful (class III).

Reference:

1. Guidelines for the diagnosis and management of syncope (version 2009) The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). European Heart Journal (2009) 30, 2631–2671

Answer: C

Keywords: Cardiology review, Cardiology, Multiple choice questions, medical tudents, Electrophysiology,  Syncope