COMPLETE
HEART BLOCK
Dr.Nagula Praveen
Perspective of Chronic heart block in Eastern India, Manotosh Panja
PERSPECTIVE
• Chronic AV block significant problem
• Increased economic burden as increased use of PPI
needed.
• Geographical variation in prevalence – 42% population
(Eastern India)
• Symptomatic AV block – 5th to 6th decade, middle class
smokers, sedentary life style.
North zone 15%
Central zone 15%
West zone 10%
South zone 18%
Clinical correlations
1.Coronary artery disease
• 15/100 cases (pathology) are due to ischemia – Davies et al.
• Sidden and simons – no more than 20% cases due to IHD.
• Panja et al – 20% cases IHD
• Histopathologically – atherosclerotic changes of the coronary artery thrombosis of
intraluminal vessels.
• MI – Ischemia CHB
• Nodal artery – main bundle destruction (Fulconer and Dean)
• Fibrosis and calcification of the ventricular septum that involves the branching part
of the AV bundle and LBBB – genesis of conduction defect.
Demographic profile
Mustard oil consumption 89.3%
Rapseed oil consumption 23.5%
Other oils 11.7%
Smoker 67%
Sedentary habit 90.6%
Bengalee 97.3%
Panja et al.
coronary angiography profile in CHB
– Panja et al.
• Age 35-65 years (40 years)
• Males -35,Females -15
• 3 pts < 30% obstruction, 6 pts - >70% significant obstruction
• AV nodal artery visualized in 46 cases (92%)
• Septal perforators identified in all.
• 18% cases due to ischemia
• LAD,RCA,LCX artery involved frequently.
• 41 patients had normal CAG.
2.Diabetes mellitus
• 4/50
• Proliferative changes of diabetic microangiopathy, intramural coronary vessels,
myocardial fibrosis, AV nodal, proximal bundle of His
• Increased fascicular block
• Small vessel changes – lead to CHB
• Deposition of PAS(periodic acid schiff) +ve – endothelial proliferation, basement
membrane thickening
• Small vessels – CHB, large vessel – CAD.
3.Hypertension
• Coronary arteriosclerosis or sclerosis of the left side of cardiac skeleton (increased in
hypertension)
4.Cardiomyopathy
• Idiopathic
• Secondary
• 15% DCMP
• 3% HCM
• Sarcoidosis – important cause of CHB
• Chagas disease
• AV block rarely associated with rheumatoid arthritis,common in ankylosing spondylitis.
5.valvular heart disease
• Calcific aortic stenosis
• Mitral valve disease (uncommon)
• MAC+
• AV – main HIS bundle
6.congenital heart disease
• Isolated abnormality
• CCTGA
• Atrial musculature – AV bundle(absent) – HIS bundle
• Fetal myocarditis
• Idiopathic hemorrhage and necrosis within the conducting tissue
• Degeneration and fibrosis related in some instance to transplacental passage of Anti Ro/Anti SSA
Saxena et al
• 44 cases of congenital CHB (AIIMS, Delhi)
• 31 – asymptomatic (group I),13 - syncope, near syncope, convulsions (group II)
• Ventricular rate ( 56.7 ± 13.2 beats/min vs 46.5 ± 6.0 beats/min)
• Wide QRS (2/31 vs 2/13)
• Pauses > 3 sec – infrequent in both
• EP study – suprahisian block on ECG
• Corrected junctional recovery time – no significance
• HR<50/min (during waking hours)
• Wide QRS escape rhythm
• Pause > 3 seconds
PPM
• 7. Degenerative disease
• Lev and lenegre
• Impaired function of conduction system
• Degenerative, fibrous changes
• From outside - Lev’s disease
• Primary degeneration – Lenegre disease
• 46/100 cases – Davies et al
• 8/15 cases – Panja et al
Erucic acid – The culprit of mustard
oil
• 1-10% of total fatty acids
• Increased concentration in mustard oil
• Sen et al – Human hearts, Bengalees
• Erucic acid was found in normal atheroscleortic heart muscle
• Increased esterified cholesterol (↑DOHA)
• Increased phosphatidyl choline
• Increased sphingomyelin
• Decreased phosphatidyl ethanolamine
• Decreased cardiolipin
• Decreased linoleic acid ( damaged by erucic acid) – inhibits oxidation of long chain fatty
acids – increased TG synthesis, increased cholesterol eructitate
• Lipidosis- acute effect of the mustard oil feedings
• increased collagen synthesis - long term effect
Panja et al
Histopathology Primary HTN/OHD Diabetes
Myocardial fibrosis 8 0 1
AV nodal with HIS
bundle fibrosis
5 1 2
Small vessel change 0 0 3
Atherosclerotic changes 0 4 0
Causes of chronic AV block – Davies et al
100 cases
Idiopathic bilateral branch fibrosis 46%
Ischaemic coronary artery disease
Destruction of both bundle branches 14%
Destruction of AV node 01%
Cardiomyopathy 13%
Calcific valve disease 8%
Myocarditis 4%
Connective tissue disorder 3%
Amyloidosis 3%
Transfusion siderosis only AV node affected 2%
Congenital heart block only main bundle affected 3%
Gumma of IVS 3%
Postmortem study – 15 patients
Age range 30 -90 years
idiopathic 8
IHD 3
Diabetes 4
Hypertension 4
Connective tissue disease 1
THANK YOU

Complete Heart Block

  • 1.
    COMPLETE HEART BLOCK Dr.Nagula Praveen Perspectiveof Chronic heart block in Eastern India, Manotosh Panja
  • 2.
    PERSPECTIVE • Chronic AVblock significant problem • Increased economic burden as increased use of PPI needed. • Geographical variation in prevalence – 42% population (Eastern India) • Symptomatic AV block – 5th to 6th decade, middle class smokers, sedentary life style. North zone 15% Central zone 15% West zone 10% South zone 18%
  • 3.
    Clinical correlations 1.Coronary arterydisease • 15/100 cases (pathology) are due to ischemia – Davies et al. • Sidden and simons – no more than 20% cases due to IHD. • Panja et al – 20% cases IHD • Histopathologically – atherosclerotic changes of the coronary artery thrombosis of intraluminal vessels. • MI – Ischemia CHB • Nodal artery – main bundle destruction (Fulconer and Dean) • Fibrosis and calcification of the ventricular septum that involves the branching part of the AV bundle and LBBB – genesis of conduction defect.
  • 4.
    Demographic profile Mustard oilconsumption 89.3% Rapseed oil consumption 23.5% Other oils 11.7% Smoker 67% Sedentary habit 90.6% Bengalee 97.3% Panja et al.
  • 5.
    coronary angiography profilein CHB – Panja et al. • Age 35-65 years (40 years) • Males -35,Females -15 • 3 pts < 30% obstruction, 6 pts - >70% significant obstruction • AV nodal artery visualized in 46 cases (92%) • Septal perforators identified in all. • 18% cases due to ischemia • LAD,RCA,LCX artery involved frequently. • 41 patients had normal CAG.
  • 6.
    2.Diabetes mellitus • 4/50 •Proliferative changes of diabetic microangiopathy, intramural coronary vessels, myocardial fibrosis, AV nodal, proximal bundle of His • Increased fascicular block • Small vessel changes – lead to CHB • Deposition of PAS(periodic acid schiff) +ve – endothelial proliferation, basement membrane thickening • Small vessels – CHB, large vessel – CAD.
  • 7.
    3.Hypertension • Coronary arteriosclerosisor sclerosis of the left side of cardiac skeleton (increased in hypertension) 4.Cardiomyopathy • Idiopathic • Secondary • 15% DCMP • 3% HCM • Sarcoidosis – important cause of CHB • Chagas disease • AV block rarely associated with rheumatoid arthritis,common in ankylosing spondylitis.
  • 8.
    5.valvular heart disease •Calcific aortic stenosis • Mitral valve disease (uncommon) • MAC+ • AV – main HIS bundle 6.congenital heart disease • Isolated abnormality • CCTGA • Atrial musculature – AV bundle(absent) – HIS bundle • Fetal myocarditis • Idiopathic hemorrhage and necrosis within the conducting tissue • Degeneration and fibrosis related in some instance to transplacental passage of Anti Ro/Anti SSA
  • 9.
    Saxena et al •44 cases of congenital CHB (AIIMS, Delhi) • 31 – asymptomatic (group I),13 - syncope, near syncope, convulsions (group II) • Ventricular rate ( 56.7 ± 13.2 beats/min vs 46.5 ± 6.0 beats/min) • Wide QRS (2/31 vs 2/13) • Pauses > 3 sec – infrequent in both • EP study – suprahisian block on ECG • Corrected junctional recovery time – no significance • HR<50/min (during waking hours) • Wide QRS escape rhythm • Pause > 3 seconds PPM
  • 10.
    • 7. Degenerativedisease • Lev and lenegre • Impaired function of conduction system • Degenerative, fibrous changes • From outside - Lev’s disease • Primary degeneration – Lenegre disease • 46/100 cases – Davies et al • 8/15 cases – Panja et al
  • 11.
    Erucic acid –The culprit of mustard oil • 1-10% of total fatty acids • Increased concentration in mustard oil • Sen et al – Human hearts, Bengalees • Erucic acid was found in normal atheroscleortic heart muscle • Increased esterified cholesterol (↑DOHA) • Increased phosphatidyl choline • Increased sphingomyelin • Decreased phosphatidyl ethanolamine • Decreased cardiolipin • Decreased linoleic acid ( damaged by erucic acid) – inhibits oxidation of long chain fatty acids – increased TG synthesis, increased cholesterol eructitate • Lipidosis- acute effect of the mustard oil feedings • increased collagen synthesis - long term effect
  • 12.
    Panja et al HistopathologyPrimary HTN/OHD Diabetes Myocardial fibrosis 8 0 1 AV nodal with HIS bundle fibrosis 5 1 2 Small vessel change 0 0 3 Atherosclerotic changes 0 4 0
  • 13.
    Causes of chronicAV block – Davies et al 100 cases Idiopathic bilateral branch fibrosis 46% Ischaemic coronary artery disease Destruction of both bundle branches 14% Destruction of AV node 01% Cardiomyopathy 13% Calcific valve disease 8% Myocarditis 4% Connective tissue disorder 3% Amyloidosis 3% Transfusion siderosis only AV node affected 2% Congenital heart block only main bundle affected 3% Gumma of IVS 3%
  • 14.
    Postmortem study –15 patients Age range 30 -90 years idiopathic 8 IHD 3 Diabetes 4 Hypertension 4 Connective tissue disease 1
  • 15.