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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

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

 

Revised Jones Criteria for Acute Rheumatic Fever – 2015 guideline

Acute rheumatic fever remains a serious healthcare concern for the majority of the world’s population despite its decline in incidence in Europe and North America. This statement reviews the historic Jones criteria used to diagnose acute rheumatic fever in the context of the current epidemiology of the disease and updates those criteria to also taking into account the use of Doppler echocardiography in the diagnosis of carditis as a major manifestation of acute rheumatic fever.

1. Epidemiology:

1. It is reasonable to consider individuals to be at low risk for ARF if they come from a setting or population known to experience low rates of ARF or RHD (Class IIa; Level of Evidence C).
2. It is reasonable that where reliable epidemiological data are available, low risk should be defined as having an ARF incidence <2 per 100 000 school-aged children (usually 5–14 years old) per year or an allage prevalence of RHD of ≤1 per 1000 population per year (Class IIa; Level of Evidence C).
3. Children not clearly from a low-risk population are at moderate to high risk depending on their reference population (Class I; Level of Evidence C).

2. Clinical Manifestations of ARF:

Generally, the clinical profile of ARF in low- and middle-income countries closely resembles that of high-income countries. Universally, the most common major manifestations during the first episode of ARF (the “major criteria” for diagnosis) remain
carditis (50%–70%) and arthritis (35%–66%). These are followed in frequency by chorea (10%–30%), which has been demonstrated to have a female predominance, and then
subcutaneous nodules (0%–10%) and erythema marginatum (<6%), which remain much less common but highly specific manifestations of ARF.

3.Carditis: Diagnosis in the Era of Widely Available Echocardiography:

Classically, as discussed in the 1992 AHA revised Jones criteria statement, carditis as a major manifestation of ARF has been a clinical diagnosis based on the auscultation of typical murmurs that indicate mitral or aortic valve regurgitation, at either valve or both valves. Numerous studies over the past 20 years have addressed the role of echocardiography (compared with purely clinical assessment) in the diagnosis of ARF. More than 25 studies have reported echocardiography/Doppler evidence of mitral or aortic valve regurgitation in patients with ARF despite the absence of classic auscultatory findings. This writing group concludes the following:

1. Echocardiography with Doppler should be performed in all cases of confirmed and suspected ARF (Class I; Level of Evidence B).
2. It is reasonable to consider performing serial echocardiography/ Doppler studies in any patient with diagnosed or suspected ARF even if documented carditis is not present on diagnosis (Class IIa; Level of Evidence C).
3. Echocardiography/Doppler testing should be performed to assess whether carditis is present in the absence of auscultatory findings, particularly in moderate- to high-risk populations and when ARF is considered likely (Class I; Level of Evidence B).
4. Echocardiography/Doppler findings not consistent with carditis should exclude that diagnosis in patients with a heart murmur otherwise thought to indicate rheumatic carditis (Class I; Level of Evidence B).

Evolving role of echogardiography in acute rheumatic fever

Evolving role of echogardiography in acute rheumatic fever

4.Specific doppler criteria for diagnosis of rheumatic valvulitis

Pathological mitral regurgitation (all 4 criteria met)
1.Seen in at least 2 views
2.Jet length ≥2 cm in at least 1 view
3.Peak velocity >3 m/s
4.Pansystolic jet in at least 1 envelope

Pathological aortic regurgitation (all 4 criteria met)
1.Seen in at least 2 views
2.Jet length ≥1 cm in at least 1 view
3.Peak velocity >3 m/s
4.Pan diastolic jet in at least 1 envelope

Morphological Findings on Echocardiogram in Rheumatic Valvulitis

Acute mitral valve changes
Annular dilation
Chordal elongation
Chordal rupture resulting in flail leaflet with severe mitral regurgitation
Anterior (or less commonly posterior) leaflet tip prolapse
Beading/nodularity of leaflet tips

Chronic mitral valve changes: not seen in acute carditis
Leaflet thickening
Chordal thickening and fusion
Restricted leaflet motion
Calcification

Aortic valve changes in either acute or chronic carditis
Irregular or focal leaflet thickening
Coaptation defect
Restricted leaflet motion
Leaflet prolapse

5.Evidence of preceding Streptococcal infection:

Because other illnesses may closely resemble ARF, laboratory evidence of antecedent group A streptococcal infection is needed whenever possible, and the diagnosis is in doubt when such evidence is not available.

Any one of the following can serve as evidence of preceding infection:
Increased or rising anti-streptolysin O titer or other streptococcal antibodies (anti-DNASE B) (Class I, Level of Evidence B). A rise in titer is better evidence than a single titer result.
A positive throat culture for group A β-hemolytic streptococci (Class I, Level of Evidence B).
A positive rapid group A streptococcal carbohydrate antigen test in a child whose clinical presentation suggests a high pretest probability of streptococcal pharyngitis (Class I, Level of Evidence B).

6. Diagnosis of Acute rheumatic fever:

For all patient populations with evidence of preceding GAS infection

Diagnosis: initial ARF: 2 Major manifestations or 1 major plus 2 minor manifestations
Diagnosis: recurrent ARF: 2 Major or 1 major and 2 minor or 3 minor

Major and minor criteria for diagnosis of Acute rheumatic fever

Major and minor criteria for diagnosis of Acute rheumatic fever


Flow charts for diagnosis of rheumatic fever

Flow charts for diagnosis of rheumatic fever

 

7.Rheumatic Fever Recurrences

As stated in the 1992 guidelines, patients who have a history of ARF or RHD are at high risk for “recurrent” attacks if reinfected with group A streptococci. Such an attack is considered
a new episode of ARF, but one in which the complete set of Jones criteria, even as revised, may not be completely fulfilled.

The guideline recommendations for diagnosing rheumatic fever recurrences are:
1. With a reliable past history of ARF or established RHD, and in the face of documented group A streptococcal infection, 2 major or 1 major and 2 minor or 3 minor manifestations may be sufficient for a presumptive diagnosis (Class IIb; Level of Evidence C).
2. When minor manifestations alone are present, the exclusion of other more likely causes of the clinical presentation is recommended before a diagnosis of an ARF recurrence is made (Class I; Level of Evidence C).

8.“Possible” Rheumatic Fever

In some circumstances, a given clinical presentation may not fulfill these updated Jones criteria, but the clinician may still have good reason to suspect that ARF is the diagnosis.
This may occur in high-incidence settings. In such situations the clinicians should use their discretion and clinical acumen to make the diagnosis that they consider most likely and manage the patient accordingly.

1. Where there is genuine uncertainty, it is reasonable to consider offering 12 months of secondary prophylaxis followed by reevaluation to include a careful history and physical examination in addition to a repeat echocardiogram (Class IIa; Level of Evidence C).
2. In a patient with recurrent symptoms (particularly involving the joints) who has been adherent to prophylaxis recommendations but lacks serological evidence of group A streptococcal infection and lacks echocardiographic evidence of valvulitis, it is reasonable
to conclude that the recurrent symptoms are not likely related to ARF, and discontinuation of antibiotic prophylaxis may be appropriate (Class IIa; Level of Evidence C).

Summary:

Jones criteria needed revision to meet current technological advances and clinical needs. Strict application of echocardiography/Doppler findings may be used to fulfill the major criterion of carditis, even in the absence of classic auscultatory findings, providing that ambient loading conditions are taken into consideration. In addition, monoarthritis or polyarthralgia could be accepted as fulfilling the major criterion of arthritis, but only in moderate- to high-risk populations. For low-risk populations, monoarthritis is not included, and polyarthralgia remains a minor criterion. Similarly, the requirement for the presence of fever can be fulfilled with oral, tympanic, or rectal temperature documented at 38°C in moderate- to high-risk populations, but only at ≥38.5°C in others.

Refernce:

1. http://circ.ahajournals.org/content/early/2015/04/23/CIR.0000000000000205.abstract

Top 10 Cardiology Articles of the week

Top 10 Cardiology Articles of the week (02.03.2015-08.03.2015)

1. Low-Level Transcutaneous Electrical Vagus Nerve Stimulation (LLTS) Suppresses Atrial Fibrillation

Conclusion: LLTS suppresses AF and decreases inflammatory cytokines in patients with paroxysmal AF. The results support the emerging paradigm of neuromodulation to treat AF.

2. Implantable Cardioverter-Defibrillator Therapy in Brugada Syndrome:A 20-Year Single-Center Experience

Background: Patients with Brugada syndrome and aborted sudden cardiac death or syncope have higher risks for ventricular arrhythmias (VAs) and should undergo implantable cardioverter-defibrillator (ICD) placement. Device-based management of asymptomatic patients is controversial. ICD therapy is associated with high rates of inappropriate shocks and device-related complications.

Objectives: The objective of this study was to investigate clinical features, management, and long-term follow-up of ICD therapy in patients with Brugada syndrome.

Methods: Patients presenting with spontaneous or drug-induced Brugada type 1 electrocardiographic findings, who underwent ICD implantation and continuous follow-up at a single institution, were eligible for this study.

Results A total of 176 consecutive patients were included. During a mean follow-up period of 83.8 ± 57.3 months, spontaneous sustained VAs occurred in 30 patients (17%). Eight patients (4.5%) died. Appropriate ICD shocks occurred in 28 patients (15.9%), and 33 patients (18.7%) had inappropriate shocks. Electrical storm occurred in 4 subjects (2.3%). Twenty-eight patients (15.9%) experienced device-related complications. In multivariate Cox regression analysis, aborted sudden cardiac death and VA inducibility on electrophysiologic studies were independent predictors of appropriate shock occurrence.

Conclusions: ICD therapy was an effective strategy in Brugada syndrome, treating potentially lethal arrhythmias in 17% of patients during long-term follow-up. Appropriate shocks were significantly associated with the presence of aborted sudden cardiac death but also occurred in 13% of asymptomatic patients. Risk stratification by electrophysiologic study may identify asymptomatic patients at risk for arrhythmic events and could be helpful in investigating syncope not related to VAs. ICD placement is frequently associated with device-related complications, and rates of inappropriate shocks remain high regardless of careful device programming.

3.Evaluation and Treatment of Patients With Lower Extremity Peripheral Artery Disease

The lack of consistent definitions and nomenclature across clinical trials of novel devices, drugs, or biologics poses a significant barrier to accrual of knowledge in and across peripheral artery disease therapies and technologies. Recognizing this problem, the Peripheral Academic Research Consortium, together with the U.S. Food and Drug Administration and the Japanese Pharmaceuticals and Medical Devices Agency, has developed a series of pragmatic consensus definitions for patients being treated for peripheral artery disease affecting the lower extremities. These consensus definitions include the clinical presentation, anatomic depiction, interventional outcomes, surrogate imaging and physiological follow-up, and clinical outcomes of patients with lower-extremity peripheral artery disease. Consistent application of these definitions in clinical trials evaluating novel revascularization technologies should result in more efficient regulatory evaluation and best practice guidelines to inform clinical decisions in patients with lower extremity peripheral artery disease.

4. Long-Term Survival Benefit of Revascularization Compared With Medical Therapy in Patients With Coronary Chronic Total Occlusion and Well-Developed Collateral Circulation

Objectives: The purpose of this study was to compare the long-term clinical outcomes of patients with chronic total occlusion (CTO) and well-developed collateral circulation treated with revascularization versus medical therapy.

Background: Little is known about the clinical outcomes and optimal treatment strategies of CTO with well-developed collateral circulation.

Methods: 2,024 consecutive patients with at least 1 CTO detected on coronary angiogram were screened. Of these, data was analyzed from 738 patients with Rentrop 3 grade collateral circulation who were treated with medical therapy alone (n = 236), coronary artery bypass grafting (n = 170) or percutaneous coronary intervention (n = 332; 80.1% successful). Patients who underwent revascularization and medical therapy (revascularization group, n = 502) were compared with those who underwent medical therapy alone (medication group, n = 236) in terms of cardiac death and major adverse cardiac events (MACE), defined as the composite of cardiac death, myocardial infarction, and repeat revascularization.

Results: During a median follow-up duration of 42 months, multivariate analysis revealed a significantly lower incidence of cardiac death (hazard ratio [HR]: 0.29; 95% confidence interval [CI]: 0.15 to 0.58; p < 0.01) and MACE (HR: 0.32; 95% CI: 0.21 to 0.49; p < 0.01) in the revascularization group compared with the medication group. After propensity score matching, the incidence of cardiac death (HR: 0.27; 95% CI: 0.09 to 0.80; p = 0.02) and MACE (HR: 0.44; 95% CI: 0.23 to 0.82; p = 0.01) were still significantly lower in the revascularization group than in the medication group.

Conclusions In patients with coronary CTO and well-developed collateral circulation, aggressive revascularization may reduce the risk of cardiac mortality and MACE.

5.Percutaneous Circulatory Assist Devices for High-Risk Coronary Intervention

A unifying definition of what constitutes high-risk percutaneous coronary intervention remains elusive. This reflects the existence of several recognized patient, anatomic, and procedural characteristics that, when combined, can contribute to elevating risk. The relative inability to withstand the adverse hemodynamic sequelae of dysrhythmia, transient episodes of ischemia-reperfusion injury, or distal embolization of atherogenic material associated with coronary intervention serve as a common thread to tie this patient cohort together. This enhanced susceptibility to catastrophic hemodynamic collapse has triggered the development of percutaneous cardiac assist devices such as the intra-aortic balloon pump, Impella (Abiomed Inc., Danvers, Massachusetts), TandemHeart (CardiacAssist, Inc., Pittsburgh, Pennsylvania), and extracorporeal membranous oxygenation to provide adjunctive mechanical circulatory support. In this state-of-the-art review, we discuss the physiology underpinning their application. Thereafter, we examine the results of several randomized multicenter trials investigating their use in high-risk coronary intervention to determine which patients would benefit most from their implantation and whether there is a signal to delineate whether they should be used in an elective pre-procedure, standby, rescue, or routine post-procedure fashion.

6.Porcelain Aorta: A Comprehensive Review

Calcification of the thoracic aorta is often associated with valvular and coronary calcification, reflecting an underlying atherosclerotic process. It has been found to be associated with an increased rate of mortality and cardiovascular disease. Porcelain aorta (PA) is extensive calcification of the ascending aorta or aortic arch that can be completely or near completely circumferential. This entity is rare in the general population, but it has an increasing incidence in older patients and in patients with coronary artery disease (CAD) or aortic stenosis (AS). The clinical relevance is based on the fact that it can complicate surgical aortic valve replacement (SAVR) for the treatment of severe AS by preventing safe access via the ascending aorta. PA is associated with increased morbidity and mortality, especially as a result of increased perioperative stroke risk. Recently, transcatheter aortic valve replacement (TAVR) has emerged as a less invasive and feasible treatment option in patients at high risk for conventional SAVR. In some series, ≈20% (5%–33%) of patients undergoing TAVR were diagnosed with PA. Inconsistencies in the definition and the use of different diagnostic modalities contribute to this wide range of PA prevalence. This article reviewed the available published data to seek a consistent, clinically relevant definition based on contemporary imaging, a firm understanding of the pathogenesis and associations, and the clinical implications of this disease entity.

7.Digoxin use in patients with atrial fibrillation and adverse cardiovascular outcomes: a retrospective analysis of the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF)

Conclusion: Digoxin treatment was associated with a significant increase in all-cause mortality, vascular death, and sudden death in patients with AF. This association was independent of other measured prognostic factors, and although residual confounding could account for these results, these data show the possibility of digoxin having these effects. A randomised trial of digoxin in treatment of AF patients with and without heart failure is needed.

8.Diagnosis of atrial fibrillation after stroke and transient ischaemic attack: a systematic review and meta-analysis

Background:Among patients with atrial fibrillation, the risk of stroke is highest for those with a history of stroke; however, oral anticoagulants can lower the risk of recurrent stroke by two-thirds. No consensus has been reached about how atrial fibrillation should be investigated in patients with stroke, and its prevalence after a stroke remains uncertain. The authors did a systematic review and meta-analysis to estimate the proportion of patients newly diagnosed with atrial fibrillation after four sequential phases of cardiac monitoring after a stroke or transient ischaemic attack.

Methods: The authors searched PubMed, Embase, and Scopus from 1980 to June 30, 2014 and included studies that provided the number of patients with ischaemic stroke or transient ischaemic attack who were newly diagnosed with atrial fibrillation. They stratified cardiac monitoring methods into four sequential phases of screening: phase 1 (emergency room) consisted of admission electrocardiogram (ECG); phase 2 (in hospital) comprised serial ECG, continuous inpatient ECG monitoring, continuous inpatient cardiac telemetry, and in-hospital Holter monitoring; phase 3 (first ambulatory period) consisted of ambulatory Holter; and phase 4 (second ambulatory period) consisted of mobile cardiac outpatient telemetry, external loop recording, and implantable loop recording. The primary endpoint was the proportion of patients newly diagnosed with atrial fibrillation for each method and each phase, and for the sequential combination of phases. For each method and each phase, they estimated the summary proportion of patients diagnosed with post-stroke atrial fibrillation using random-effects meta-analyses.

Findings:  The systematic review returned 28 290 studies, of which 50 studies (comprising 11 658 patients) met the criteria for inclusion in the meta-analyses. The summary proportion of patients diagnosed with post-stroke atrial fibrillation was 7·7% (95% CI 5·0–10·8) in phase 1, 5·1% (3·8–6·5) in phase 2, 10·7% (5·6–17·2) in phase 3, and 16·9% (13·0–21·2) in phase 4. The overall atrial fibrillation detection yield after all phases of sequential cardiac monitoring was 23·7% (95% CI 17·2–31·0).

Interpretation: By sequentially combining cardiac monitoring methods, atrial fibrillation might be newly detected in nearly a quarter of patients with stroke or transient ischaemic attack. The overall proportion of patients with stroke who are known to have atrial fibrillation seems to be higher than previously estimated. Accordingly, more patients could be treated with oral anticoagulants and more stroke recurrences prevented.

9.Comparative Outcomes of Catheter-Directed Thrombolysis Plus Anticoagulation Versus Anticoagulation Alone in the Treatment of Inferior Vena Caval Thrombosis

Conclusions—There has been a steady increase in the use of CDT in the treatment of patients with inferior vena cava thrombosis in the United States. This observational study showed no significant difference in mortality between CDT versus anticoagulation alone; however, the bleeding events and resource utilization were higher in the CDT group. Adequately powered randomized controlled trials are needed in this area.

10.Drug-eluting stents versus bare metal stents prior to noncardiac surgery

DES implantation was not associated with higher adverse events after NCS. Moreover, the incidence of adverse events following NCS was lower when NCS was performed >90 days post-DES implantation suggesting that it may not be necessary to wait until 12 months post PCI with DES before NCS.

Calculation of heart rate from ECG

Calculation of heart rate from ECG

In my last post I have enumerated the points for studying an ECG.

The first step is to check the calibration and paper speed. Then comes the calculation of heart rate. There are various methods of calculating the heart rate from ECG. We will discuss about the most commonly used and authentic methods of calculation.

ALL THESE METHODS ARE APPLICABLE FOR PAPER SPEED OF 25MM/SEC.

No.1 and 2 are applicable for a regular heart rhythm. No.3 is applicable for irregular heart rhythm

No.1: Calculate the number of large boxes

Figure 1

Figure 1

Count the number of large boxes between two consecutive R-R waves. 300 divided by the number of large boxes between two consecutive R-R waves is the heart rate. In figure 1 there are 3 large boxes between two consecutive R-R waves, so the heart rate is 300/3 =100/minute.

No.2: Calculate the number of small boxes

Count the number of small boxes between two consecutive R-R waves. 1500 divided by the number of small boxes between two consecutive R-R waves is the heart rate. In figure 1 there are 16 small boxes between two consecutive R-R waves, so the heart rate is 1500/16 = 94/min. This method is more accurate than the previous method.

No.3: Calculate the total number of R-waves in the rhythm strip

This method is applicable when the heart rate is irregular e.g. in patients with atrial fibrillation, frequent VPCs etc. At a paper speed of 25 mm/sec the duration of a 12-lead ECG is 10 seconds. So count the total number of R-waves in the rhythm strip (the long lead II at the bottom of the ECG ) and multiply it by 6 to get the heart rate. In the example shown below there are frequent VPCs.

2011.11.8The total number of R-waves is 12. So the heart rate is 12×6 = 72/min

I suggest you practice all the methods in the beginning so that after sometime you will be well habituated to use a method as needed.

Next week we will discuss about analyzing rhythm from ECG.

CAROTID ARTERY STENTING: SILK ROAD PROCEDURE

SILK ROAD PROCEDURE

Innovation in carotid artery stenting.

Watch this nice animation to understand the concept

(downloaded from: http://www.silkroadmedical.com/silkroad-procedure/how-it-works/)

A recently presented trial (ROADSTER IDE) shows promising results for this new technique

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.