Hypertension and Arrhythmias
Feb 11, 2016
Hypertension and Arrhythmias
Introduction
Hypertension is one of the earliest recorded medical conditions Hypertension is one of the earliest recorded medical conditions (2.600BC)(2.600BC)
Consequences of hypertension will soon be the leading global Consequences of hypertension will soon be the leading global cause of deathcause of death
The risk of death increases with increasing SBPThe risk of death increases with increasing SBP
On one hand is a risk factor for the development of coronary On one hand is a risk factor for the development of coronary artery artery disease, and on the other hand for the incidence of disease, and on the other hand for the incidence of ventricular arrhythmias or even cardiac death. ventricular arrhythmias or even cardiac death.
Pathophysiology
Arrhythmias
Prediction of Risk
Treatment
Hypertension and Arrhythmias
Mechanisms regulating mean arterial blood pressure
LVH: Causative Factors
Genetic/environmental
factors
AgeGender
RaceOther illness
Hemodynamic load
Volume PressureTrophic factors
Angiotensin IIAldosterone
CatecholaminesInsulin
Arterial hypertension
Left ventricular hypertrophy
↑Fibrosis
↓Coronary flow
↑ Media hypertrophy
↑ Wall stress
Ischemia
reserve
Conduction – and depolarization disorders
Re-entry
Stretching of myocytes
Increased automaticityTriggered activity
Ventricular tachycardia
Sudden cardiac death
↑ Catecholamines
↑ Heart rate
↑ Sympathetic tone
Duration of the action potential is increased
The plateau phase of the action potential is more labile than non-LVH
Disorders of the cytosolic calcium concentrations
The normal regional differences of action potential duration are reversed
Reentry seems to be directly linked with fibrosis
Link of LV wall stress and arrhythmias
The HRV is decreased
Electrolyte imbalance such as disorders of calcium and potassium channels
Arrhythmogenic Mechanisms in Hypertension
Experimental Evidence for Beneficial Effects of Potassium
Mcdonald JE et al. J Am Coll Cardiol 2004;43: 155 Mcdonald JE et al. J Am Coll Cardiol 2004;43: 155
CardiacCardiacAnti - arrhythmicAnti - arrhythmic ↓↓ Action potential durationAction potential duration
↓↓ Electrical in homogeneityElectrical in homogeneity↓↓ Risk of digoxin toxicityRisk of digoxin toxicity
Diastolic functionDiastolic function Hypokalemia worsens diastolic functionHypokalemia worsens diastolic function
VascularVascular
VasomotorVasomotor Endothelial-dependent vasodilatorEndothelial-dependent vasodilatorVSMCVSMCThrombosisThrombosisAtherosclerosisAtherosclerosis
↓↓ VSMC proliferationVSMC proliferation↓↓ Thrombus formation and platelet activationThrombus formation and platelet activation↓↓ Neointimal proliferationNeointimal proliferation↓↓ Atherosclerotic lesion formationAtherosclerotic lesion formation↓↓ Free radical generationFree radical generation
VSMC = vascular smooth muscle cell.VSMC = vascular smooth muscle cell.
Attenuated Coronary Flow Reserve and Vascular Remodeling in Patients With Hypertension and Left Ventricular Hypertrophy
Coronary Hemodynamic Characteristics
n=6848.1 ±3.22.8 ±0.1 2.9 ±0.2
69.8 ±6.8
56.1 ±13.1
-12.3 ±4.2
n=3056.5 ±6.2 2.7 ±0.12.7 ±0.3
78.1 ±11.5
46.9 ±20.2
-11.3 ±5.4
n=1381.1 ±9.9*† 2.3 ±0.2*†1.7 ±0.3*‡
99.3 ±29.0
1.5 ±20.5†
-31.6 ±9.5
No.of patientsCBF at baseline(ml/min)Coronary flow reserve to adenosineCoronary vascular resistance(mm Hg min/ml)CBF change induced by acetylcholine (min/ml)% change of CBF induced byAcetylcholine (%)% change of CAD induced byAcetylcholine (%)
Group 3
Normotensive
Group 2Hypertensive
Without LVH
Group 1Hypertensive
With LVH
Values are mean ± SE.CAD = coronary artery diameter; CBF = coronary blood flow; LVH = left ventricular hypertrophy.*p < 0.05 versus group 2; †p < 0.01; ‡<0.05 versus group 3. Hamasaki S. et al. J Am Coll Cardiol 2000.
Heart Rate, Mean Blood Pressure and CFR Changes After Clonidine Infusion
0
20
40
60
80
100
120
HR MBP
Baseline Post Clonidine
2.9
3
3.1
3.2
CFR
*
* p < . 01
*
CORONARY FLOW RESERVE CHANGES FOLLOWING CLONIDINE INFUSION
Voudris V, Manolis AJ et al Am J Hypertens 2003
Hemodynamic and Humoral Correlates in Essential HTN:
Relationship Between Patterns of LVH and Myocardial Ischemia
Manolis AJ et al. Hypertension. 1997
ETT (-)ETT (-) ETT(+), Th(+), CA(-)ETT(+), Th(+), CA(-)
Holter: (+), Holter: (+), HRV: (+), LPs: (+)HRV: (+), LPs: (+)NE: p:NSNE: p:NS
Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and HF
MSNA responses to spontaneous PVCs are similar in controls and EH but MSNA responses to spontaneous PVCs are similar in controls and EH but markedly impaired in CHF, presumably because of the baroreflex alteration markedly impaired in CHF, presumably because of the baroreflex alteration
Grassi G et al. Hypertension 2002; 39:886Grassi G et al. Hypertension 2002; 39:886
Renin-Angiotensin Aldosterone System
Angiotensinogen
Non-ACE pathways(eg, chymase)
Vasoconstriction Cell growth Na/H2O retention Sympathetic activation
Renin Angiotensin I
Angiotensin II
ACE
Cough,angioedema
Benefits? Bradykinin Inactive
fragments
Vasodilation Antiproliferation
(kinins)
Aldosterone AT2
AT1
Pathophysiology
Arrhythmias
Prediction of Risk
Treatment
1919thth Annual Scientific Meeting of the American Society of Hypertension Annual Scientific Meeting of the American Society of Hypertension
Hypertension and Arrhythmias
Ventricular ectopy in patients with normal left ventricular (LV) mass and left ventricular hypertrophy
Novo S. et al. Am J Hypertens 1997;10:843Novo S. et al. Am J Hypertens 1997;10:843
Percentage of Patients with Supraventricular and Ventricular Arrhythmias in Hypertensives with or without LVH
Novo S. et al. Am J hypertens 1997;10:843Novo S. et al. Am J hypertens 1997;10:843
Coefficients of Correlation (R) Between SBP, DBP, HR and Supraventricular and Ventricular Arrhythmias in two
Groups of Hypertensives with or without LVH
With LVHWith LVH Without LVHWithout LVH
PSVBPSVB PVBPVB PSVBPSVB PVBPVB
ASBPASBP 0.340.34 0.83*0.83* 0.88*0.88* 0.380.38
ADBPADBP 0.390.39 0.74*0.74* 0.49*0.49* 0.310.31
AHRAHR 0.55*0.55* 0.87*0.87* 0.76*0.76* 0.360.36* p<.01* p<.01
Associations of Systolic and Diastolic Blood Pressure with Prevalence of Atrial Fibrillation
Ciaroni S et al. Am J Cardiol 2004;94:2566Ciaroni S et al. Am J Cardiol 2004;94:2566
OR (95% CI)OR (95% CI)
VariablesVariables Systolic BPSystolic BP(per 10mm Hg)(per 10mm Hg)
Diastolic BP Diastolic BP (per 10mm Hg)(per 10mm Hg)
Pulse Pressure Pulse Pressure (per 9 mm Hg)(per 9 mm Hg)
UnadjustedUnadjusted 1.46*1.46* 1.071.07 1.52*1.52*
AdjustmentAdjustment
Age (5 yrs)Age (5 yrs) 1.25*1.25* 1.051.05 1.23*1.23*
Age and gender (men)Age and gender (men) 1.21*1.21* 1.041.04 1.19*1.19*
Age, gender and BMI (>28kg/mAge, gender and BMI (>28kg/m22)) 1.16*1.16* 1.021.02 1.18*1.18*
Age, gender, BMI and systolic BPAge, gender, BMI and systolic BP -- 1.011.01 1.171.17
Age, gender, BMI and pulse pressureAge, gender, BMI and pulse pressure 1.15*1.15* 0.910.91 --
*p < 0.001*p < 0.001
Factors Associated With Ischemic Stroke Multivariate Analysis SPAF I-III Trial
Hart R.G. et al. Stroke. 1999; 30: 1223-1229 Hart R.G. et al. Stroke. 1999; 30: 1223-1229
Age
Diurnal and nocturnal BP
Max duration of the depression of P wave in the ECG
LVMI
Left atrial dimension
Velocity of the A wave
Minimum P wave velocity
Predictive parameters for the onset of AF
Pathophysiology
Arrhythmias
Prediction of Risk
Treatment
Hypertension and Arrhythmias
Electrocardiographic and Signal-Averaged Data
Gatzoulis KA et al. Am J Hypertens 2000; 13: 340Gatzoulis KA et al. Am J Hypertens 2000; 13: 340
No LVHNo LVH LVHLVH PPMean HR (bpm)Mean HR (bpm) 77.6 77.6 ++ 26 26 68.8 68.8 ++ 9 9 NSNSMax HR (bpm)Max HR (bpm) 121.6 121.6 ++ 29 29 123 123 ++ 25 25 NSNSMin HR (bpm)Min HR (bpm) 51.4 51.4 ++ 13 13 52 52 ++ 10 10 NSNSPVC/hPVC/h 6.8 6.8 ++ 21 21 6 6 ++ 19 19 NSNSMultiform PVC (%)Multiform PVC (%) 7.4%7.4% 7.8%7.8% NSNSR-on-T (%)R-on-T (%) 0%0% 1%1% NSNSVVcoupcoup/24 h/24 h 0.2 0.2 ++ 1 1 0.04 – 0.20.04 – 0.2 NSNS
VTVTrunsruns/24 h/24 h 00 00 NSNS
FQRS (mc)FQRS (mc) 94 + 2094 + 20 98 + 1198 + 11 NSNSLAS (ms)LAS (ms) 28.5 + 1028.5 + 10 29.3 + 1029.3 + 10 NSNSRMS (RMS (μμV)V) 47 + 4447 + 44 46 + 3446 + 34 NSNS(+) LPs (%)(+) LPs (%) 35.4%35.4% 33.3%33.3% NSNS
Signal-Averaged ECG Parameters and Ventricular Repolarization
Facchini M et al. J Hypertens 2000; 18: 763Facchini M et al. J Hypertens 2000; 18: 763
HH HAHA CC CACA PP
QRSd (ms)QRSd (ms) 98 98 ++ 13 13 96 96 ++ 18 18 97 97 ++ 7 7 97 97 ++ 11 11 NSNS
RMS 40 (RMS 40 (μμV)V) 44 44 ++ 29 29 49 49 ++ 31 31 48 48 ++ 27 27 45 45 ++ 23 23 NSNS
LAS (ms)LAS (ms) 29 29 ++ 8 8 25 25 ++ 7 7 27 27 ++ 9 9 27 27 ++ 9 9 NSNS
LP (%)LP (%) 5%5% 3% 3% 0%0% 2%2% NSNS
QTcQTc 422 422 ++ 25 25 427 427 ++ 27 27 382 382 ++ 20 20 401 401 ++ 28 28 <.0001<.0001
QT > 440msQT > 440ms 4/19 (21%)4/19 (21%) 9/30 (30%)9/30 (30%) 0/28 (0%)0/28 (0%) 3/61 (5%)3/61 (5%) <.001<.001
QTdQTd 33 33 ++ 14 14 41 41 ++ 24 24 31 31 ++ 12 12 47 47 ++ 21 21 <.05<.05
QTd > 65msQTd > 65ms 0/19 (0%)0/19 (0%) 6/30 (20%)6/30 (20%) 0/28 (%)0/28 (%) 7/61 (11%)7/61 (11%) <.05<.05
H: HTN no arrhythmia, HA: HTN with arrhythmia, C: no HTN no arrhythmia, CA: no HTN with arrhythmiaH: HTN no arrhythmia, HA: HTN with arrhythmia, C: no HTN no arrhythmia, CA: no HTN with arrhythmia
Relative risk of non- invasive parameters concerning cardiac mortality and sudden cardiac death (univariate analysis).
The only significant parameter in the multivariate analysis was Lown-class IVB
Galinier M et al. Eur Heart J 1997;18:1484Galinier M et al. Eur Heart J 1997;18:1484
MortalityMortality Sudden cardiac deathSudden cardiac deathParameterParameter PP RRRR PP RRRR
Age > 65 yearsAge > 65 years 0.0010.001 5.315.31 0.0020.002 12.112.1
Lown IvbLown Ivb 0.00240.0024 4.374.37 0.00040.0004 17.117.1
QTd> 80 msQTd> 80 ms 0.00020.0002 5.875.87 0.010.01 4.84.8
LVEF < 65%LVEF < 65% 0.430.43 1.821.82 0.320.32 1.71.7
VLPVLP 0.530.53 1.521.52 0.970.97 1.041.04
LVH (echo)LVH (echo) 0.0020.002 4.974.97 0.340.34 1.931.93
VLP: Ventricular Late Potentials; QTd: QT-dispersionVLP: Ventricular Late Potentials; QTd: QT-dispersion
Pathophysiology
Arrhythmias
Prediction of Risk
Treatment
Hypertension and Arrhythmias
Biochemical Results
Chlorthalidone Amlodipine LisinoprilSerum cholesterol- mg/dL
Baseline 216.1 (43.8) 216.5 (44.1) 215.6 (42.4)4 Years 197.2 (42.1) 195.6 (41.0)* 195.0 (40.6)*
Serum potassium – mmol/LBaseline 4.3 (0.7) 4.3 (0.7) 4.4 (0.7)*4 Years 4.1 (0.7) 4.4 (0.7)* 4.5 (0.7)*
Estimated GFR† – mL/min/1.73m2
Baseline 77.6 (19.7) 78.0 (19.7) 77.7 (19.9)4 Years 70.0 (19.7) 75.1 (20.7)* 70.7 (20.1)*
* p<.05 compared to chlorthalidone† Ann Intern Med. 1999;130:461-470
ALLHAT
Gatzoulis K. et al. Am J Hypertension 2000.Gatzoulis K. et al. Am J Hypertension 2000.
Drug Treatment and Potassium
SHEP Trial:SHEP Trial: 7.2% of subjects taking diuretic developed 7.2% of subjects taking diuretic developed hypokalemia and they lost the cardioprotective effect of BP hypokalemia and they lost the cardioprotective effect of BP reductionreduction
MRFIT Trial:MRFIT Trial: patients who received higher doses of diuretics had patients who received higher doses of diuretics had increased risk of SCD, especially those with ECG LVH, and increased risk of SCD, especially those with ECG LVH, and for 1 mmol/l reduction of serum potassium, ventricular for 1 mmol/l reduction of serum potassium, ventricular arrhythmias increased by 28%.arrhythmias increased by 28%.
MRC Trial:MRC Trial: ventricular ectopy was unaffected by thiazide therapy ventricular ectopy was unaffected by thiazide therapy after 2 months, but was increased after 2 years and was after 2 months, but was increased after 2 years and was related to hypokalemia. related to hypokalemia.
Clinical Evidence for Beneficial Effects of Potassium and Recommended Targets for Serum Potassium Concentration
in Cardiovascular Disorders
DisorderDisorder RecommendedRecommendedLevelLevel
EvidenceEvidence
HypertensionHypertension 3.5 – 5.0 mmol/l3.5 – 5.0 mmol/l High KHigh K++ diet diet ↓↓ BP BPHypokalemia ↑ ventricular arrhythmiaHypokalemia ↑ ventricular arrhythmia
StrokeStroke UnknownUnknown High KHigh K++ diet diet ↓↓ risk of stroke risk of stroke
Acute MIAcute MI 4.5 – 5.5 mmol/l4.5 – 5.5 mmol/l Hypokalemia ↑ ventricular arrhythmiaHypokalemia ↑ ventricular arrhythmia
Heart failureHeart failure 4.5 – 5.5% mmol/l4.5 – 5.5% mmol/l Hypokalemia ↑ ventricular arrhythmiaHypokalemia ↑ ventricular arrhythmiaIncreasing serum KIncreasing serum K++ ↓↓ ventricular ventricular
arrhythmia and arrhythmia and ↓↓ QT QT QT QTdd
Serum KSerum K++ level is inversely related to level is inversely related to prognosisprognosis
BP = Blood pressure; MI = myocardial infractionBP = Blood pressure; MI = myocardial infraction
Mcdonald JE et al. J Am Coll Cardiol 2004;43: 155 Mcdonald JE et al. J Am Coll Cardiol 2004;43: 155
Symptomatic Treatment of Cardiac Arrhythmias
HTN and/or LVH suffering Supraventricular arrhythmias and AFHTN and/or LVH suffering Supraventricular arrhythmias and AF
First line:First line: class Ic (propaphenone, Flecainide, except low EF) class Ic (propaphenone, Flecainide, except low EF)
Avoid:Avoid: class III (amiodarone, sotalol )and class Ia (quinidine, class III (amiodarone, sotalol )and class Ia (quinidine, disopyramide) and Drugs increasing QT interval disopyramide) and Drugs increasing QT interval
Sotalol: 5-8% torsades de-points tachydardia Sotalol: 5-8% torsades de-points tachydardia (Hohnloser et al. N Engl J Med 1994)(Hohnloser et al. N Engl J Med 1994)
Propafenone effective in terminating SVT and AF in 84%Propafenone effective in terminating SVT and AF in 84%(Reimold SC et a. Am J Cardiol 1998)(Reimold SC et a. Am J Cardiol 1998)
If class Ic agents are not effective: amiodarone If class Ic agents are not effective: amiodarone (Podril PJ. Ann Intern Med 1995)(Podril PJ. Ann Intern Med 1995)
If Pharmacologic therapy has failedIf Pharmacologic therapy has failed
Modulation of AV-node or ablation of AV-node and pacemakerModulation of AV-node or ablation of AV-node and pacemaker
permanent atrial pacingpermanent atrial pacing
radiofrequence ablationradiofrequence ablation
ACE inhibitors Clonidine
Diuretics
Calcium channel-blockers
Beta-blockers
Improvement of QT-dispersion
Reduction of ventricular premature beats
Normalization of ventricular
electrophysiology behaviour in animal model
Regression of Hypertrophy
Reduction of sudden cardiac death?
Meta-analysis of randomized, controlled trials of LV hypertrophy regression in essential hypertension
Schmieder RE et al. Am J Med 2003; 115:41-6.
-16
-14
-12
-10
-8
-6
-4
-2
0Diuretics -blockers
Ca-antagonist
ACE-inhibitors ARBs
-8%
-6%
-11%-10%
-13%
LV m
ass
Red
uctio
n (%
)
80 randomized controlled trials;4,113 patients
ISRISR
SPIRSPIR
ISR+SPIRISR+SPIR
% SBP% SBP
(mmHg)(mmHg)
-11.6-11.6++8*8*
-11.4-11.4++7*7*
-18-18++10*10*
% DBP% DBP
(mmHg)(mmHg)
-15-15++18*18*
-14-14++6*6*
-20-20++6*6*
% LVMI% LVMI
(g/M2)(g/M2)
-7.9-7.9++44++
-9.6-9.6++8*8*
-7.8+10-7.8+10++
% NE% NE
(ng/ml)(ng/ml)
3131++7272
-7.8-7.8++7070
4444++9696
*p<0.001, *p<0.001, ++p<0.05p<0.05
% PRA% PRA
(ng/ml/hr)(ng/ml/hr)
186186++213213
192192++267267
115115++113113
% AVP% AVP
(pg/ml)(pg/ml)
236236++259259
411411++772772++
120120++336336
Comparison of Spirapril Isradipine and their Combination in HTN Patients with LVH:
Effects on LVH Regression and Arrhythmogenic Propensity
Manolis AJ et al. Am J Hypertens 1998Manolis AJ et al. Am J Hypertens 1998
PCA: Periarteriolar collagen areaTIC: Total Interstitial Collagen
* p < 0,04# p < 0.001
% Morphological and Haemodynamic changes before and after treatment.
Hypertension 2000
Repair of Coronary Arterioles After Treatment with Perindopril in Hypertensive Heart Disease
LVMICBF CVR CR PCA TIC
12%
54%
33%
67%
54%
22%
70
-70
#
#
#
*
*
*
0
Occurrence of Atrial Fibrillation According to Antihypertension Treatment: IR per 1,000 Person-Years of Atrial Fibrillation – Related
Hospitalization, Adjusted Incidence Ratio, and 95% CI
Matched CohortsMatched Cohorts ACEI IRACEI IR CCB IR CCB IR ACEI Versus CCB ACEI Versus CCB Ration (95% CI)*Ration (95% CI)*
Three yearsThree years 7.77.7 11.811.8 0.65 (0.54 – 0.83)0.65 (0.54 – 0.83)
Five yearsFive years 8.88.8 11.911.9 0.74 (0.61 – 0.89)0.74 (0.61 – 0.89)
Entire follow – upEntire follow – up 8.58.5 11.911.9 0.74 (0.62 – 0.89)0.74 (0.62 – 0.89)*Poisson regression*Poisson regression
L’Allier PL et al. J Am Coll Cardiol 2004L’Allier PL et al. J Am Coll Cardiol 2004
Incidence rate of AF-related hospitalizationsIncidence rate of AF-related hospitalizations
ACE-Inhibition in HTN Patients is Associated with a Reduction in the Occurrence of Atrial Fibrillation
Kaplan-Meir curves for the time to first occurrence of AFKaplan-Meir curves for the time to first occurrence of AFL’Allier PL et al. J Am Coll Cardiol 2004L’Allier PL et al. J Am Coll Cardiol 2004
LIFE Study Change in Cornell Voltage Duration Product and Sokolow-Lyon
-18-16
-14-12
-10-8
-6-4
-20
Cornell Product Sokolow-Lyon
Cha
nge
from
bas
elin
e (%
)
LosartanAtenolol
P<0.0001
P<0.0001
LIFE Study Primary Composite Endpoint
0 6 12 18 24 30 36 42 48 54 60 66Losartan (n) 4605 4524 4460 4392 4312 4247 4189 4112 4047 3897 1889 901Atenolol (n) 4588 4494 4414 4349 4289 4205 4135 4066 3992 3821 1854 876
Study Month
Prop
ortio
n of
pat
ient
s w
ith fi
rst e
vent
(%)
Intention-to-treat
Losartan
Atenolol
2
4
6
8
10
12
14
16
Adjusted risk reduction 13·0%, P=0·021Unadjusted risk reduction 14·6%, P=0·009
Effect of Losartan on Sudden Cardiac Death
in People with Diabetes: Data From the LIFE Study
CV Death CHD Death Sudden Death Non SD Non Coronary CV Death
-60
-50
-40
-30
-20
-10
0
10
# p<0.05
Lindholm LH, et al: Lancet 2003
Adjusted HR (95% CI)
#: p< 0.03
#
Reduction in Risk of Stroke in Patients with AF
0 6 423012 18 24 36 48 54 60 66
20
25
15
10
5
0
Fatal and nonfatal stroke
Adjusted risk reduction 49%, p = 0.018
Prop
ortio
n of
pat
ient
s w
ith
first
eve
nt (%
)
Time (months)
Atenolol
Losartan
Ischemic Stroke“Mosaic of Interacting Factors”
..
Hemodynamic factors
(central and peripheral blood
pressure)
Circulating factors(glucose, insulin, RBCs, PAI, TXA2,
uric acid)
Cardiac remodeling/enlargement
Vascular remodeling
Endothelial dysfunction
Prothrombotic state
Atheroscleroticplaques
Emboli formation
Thrombus formation
Embolic occlusion
Thrombotic occlusion
Ischemic stroke
HemorrhagicHemorrhagicstrokestroke
Vascular Vascular hemorrhagehemorrhage
Plaque fragmentsPlaque rupture
How Did Losartan Reduce the Risk of Stroke “Beyond Blood Pressure”?
Cardiac remodeling/Cardiac remodeling/enlargementenlargement
Endothelial dysfunctionEndothelial dysfunction
Prothrombotic stateProthrombotic state
Vascular remodelingVascular remodeling
Reduced ECG–LVH
Improved endothelial function
Inhibition of platelet aggregationReduced proaggregatory factors
Inhibited atherosclerosis formationReduced carotid artery hypertrophy Reduced gluteal artery hypertrophy
Please refer to notes page for reference citations.
Conclusions
Patients with HTN suffer from an increased risk of arrhythmias.Patients with HTN suffer from an increased risk of arrhythmias. The arrhythmogenic causes of arrhythmias in HTN concern The arrhythmogenic causes of arrhythmias in HTN concern triggered activity with early and delayed after-triggered activity with early and delayed after- depolarizations depolarizations and re-entry. and re-entry. The mechanisms are associated with ischemia, myocardial The mechanisms are associated with ischemia, myocardial fibrosis, increased wall stress and acute changes of BP.fibrosis, increased wall stress and acute changes of BP. The predictive accuracy of non-invasive parameters is not high The predictive accuracy of non-invasive parameters is not high enoughenough A regression of LVH leads to a reduction of ventricular ectopic A regression of LVH leads to a reduction of ventricular ectopic activity, sudden death and improves CV morbidity and activity, sudden death and improves CV morbidity and mortality mortality