How to Manage the Patients with PVC s? Apr. 15 2005 Inter-Burgo Hotel, Daegu
49 2005.2.18. 3, FC II-III, Skipped beat : : LVEDD :59mm, LVESD 48mm, LVEF 35%, Absence of regional wall motion abnormalities Holter Findings Mean HR 91bpm, min HR 70bpm and max HR 151bpm PVC 19,021 beats/day 177 couplets NSVT 3 beats fastest run 152 bpm at 21:50 Modified Bruce protocol, stage 6(10.3 Mets), suggestive + PVC at rest, stage 2 and recovery phase 2005.2.23. 15574724
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49 : : Sinus and AV node function : No significant ventricular arrhythmia induced by 3 VEST at RV apex and RVOT 3 drive cycle lengths Progress: 2005. 3.14. Discharge with medication Acertil Aldactone Lasix Aspirin Cordarone 2005. 3.28. Aborted SCD
Declare the past Diagnose the present Foretell the future Aphorisms II Hippocrates 460BC to 377BC
Background : PVC 1922, Gallavardin 1 1969, Rosenbaum 2 'Rosenbaum ventricular extrasystole'. Rosenbaum reviews the classification of ventricular premature beats and adds a benign form that arises from the right ventricle and is not associated with heart disease. Ventricular extrasystoles are a common finding in patients with and without heart disease. Frequent and repetitive extrasystoles are an independent predictive factor of total mortality and sudden death in the presence of heart disease, Very frequent monomorphic ventricular complexes and even bursts of ventricular tachycardia in subjects without evidence of heart disease are generally considered benign in the presence of heart disease,. 1. Gallavardin L. Extrasistolie ventriculaire a` paroxysmes tachycardiques prolonge s. Arch Mal Coeur 1922;15:298 306. 2. Rosenbaum MB. Classification of ventricular extrasystoles according to form. J Electrocardiol 1969;2:289 98.
Premature Ventricular Contraction(PVC)
Prognosis of PVC from Right Ventricular Outflow Tract 161 pts(12 pts with cardiac diseases) Male 62 55 ± 15 yo 50 pts FU for 28.5 ± 18.1 months Results NSVT 5(10%, including 1 DCM) Sustained VT 2( 4%, including 1 CAD) Loss of PVC 4( 8%) SCD 1( 2%) Conclusion In the patients with frequent RVOT VPBs, sustained ventricular tachycardia or sudden death could develop. Therefore, careful observation is required in patients with frequent RVOT VPBs. Oh HL, Choue CW et al. Korean Circulation J 2003;33 (12):1118
Long-Term Follow-Up of Right Ventricular Monomorphic Extrasystoles Gaita F et al. J Am Coll Cardiol 2001;38:364 61 patients 15 ± 2 years(12-20 years) Clinical examination, ECG, Holter, stress test, SAECG, Echocardiography and cardiac MR (11 patients) Results 55 alive, and 6 died(no SCD) 47 patients examined had normal ECG 24 (51%), extrasystoles were no longer present 7 (15%), late potentials were present Right ventricle was normal at echocardiography. In 8 of 11 patients (73%), cardiac MR showed focal fatty replacement and other abnormalities of the right ventricle.
Cardiac MR imaging findings in patients with RVOT premature contractions 19 patients :13 males, mean: 44 years, with frequent (> 100 per hour), monomorphic (LBBB and inferior axis morphology) PVC s 10 volunteers : 4 males, mean age 36.7 years, without structural heart disease. Cardiac MR findings :Reduced wall thickness, systolic bulging, and decreased systolic thickening ED Ø of the RVOT(transverse plane) RESULTS: Mean AP Ø :39.6 ± 4.6 mm vs. 29.9 ± 4.8 mm (P < 0.01) Transverse Ø : 27.5 ± 3.8 mm vs. 20.5 ± 2.5 mm (P < 0.01) Wall motion and morphological abnormalities: 16/19 (84%) The anterolateral wall in 15/16 cases All normal subjects: normal MR imaging findings (P = 0.008) Proclemer A. Eur Heart J. 1997 Dec;18(12):2002
Long-term Outcome in Asymptomatic Men with Exercise-induced PVC 6101 asymptomatic French men (42 to 53 years of age) Free of clinically detectable cardiovascular disease A standardized graded exercise test between 1967 and 1972. N Engl J Med 2000 343:826
Long-term Outcome in Asymptomatic Men with Exercise-induced PVC Death Rates according to the Frequency of PVC N Engl J Med 2000 343:826
Frequent Ventricular Ectopy after Exercise as a Predictor of Death 29,244 pts 56 ±11 years Men 70% Mean Follow-up : 5.3years Frequent ventricular ectopy during exercise : 945 pts(3 percent) Frequent ventricular ectopy only during recovery : 589(2 percent) N Engl J Med 2003;348:781-90
HE 40 HE 100 Trichrome 100
123 I MIBG Imaging for Sympathetic Innervation 21148375PVC
42.
fqrsd 114 ms LAS40 38 ms RMS40 <20 µv
HE 40 HE 100 Trichrome 100
Modified Bruce protocol, stage 6 I V1 II V2 III V3 avr V4 avl V5 avf V6
Cause:PVC Cardiac - Myocardial ischemia or infarction - Myocarditis - Cardiomyopathy(dilated, hypertrophic) Medications - Digoxin, sympathomimetic, TCA. Substance abuse - Alcohol, tobacco, caffein, cocaine, amphetamine.. Electrolye Imbalance - Hypokalemia, hypomagnesemia, hypercalcemia Others - Anxiety or stress, fatigue
Biological model of SCD Structure Myocardial infarction Acute Healed Aneurysm Hypertrophy Secondary Primary Myopathic ventricle Dilation, fibrosis infiltration inflammation Structural electrical abnormality ELECTROGENIC THEORY PVCs? VT/VF Function Transient alteration of coronary blood flow Vasomotor dynamics Acute ischemia Reperfusion after ischemia Systemic factor Hemodynamic failure Hypoxemia, acidosis Electrolyte imbalance Neurophysiological interaction Transmitters Central influences Toxic effects Proarrhythmic drugs Cardiac toxicity
Evaluation History and PE Blood chemistry Chest PA EKG Signal-averaged ECG Holter monitoring Exercise Stress Test RI scan Cardiac electrophysiologic study
Clinical Substrates Associated with SCD Coronary artery disease Idiopathic cardiomyopathy Hypertrophic cardiomyopathy Long QT syndrome RV dysplasia Rarely: WPW syndrome
Conventional Risk Prediction Post AMI Mortality 50% Mortality 25% 0% 20% 70% 0 6 10 20 LVEF VPBs
Survival After Acute MI Bigger JT. Am J Cardiol. 1986;57:12B 1.0 Survivorship 0.8 0.6 0.4 0.2 A B C D N 536 113 80 37 EF 30% 30% < 30% < 30% VPD < 10/hr 10/hr < 10/hr 10/hr A B C D 0 1 Year 2 3
Risk of SCD in Relation to Complexity of Ventricular Arrhythmia 25 Sudden Coronary Deaths 25 Other Cardiac Deaths 20 15 10 5 Cumulative Probability of Death (age-adjusted %) 20 15 10 5 0 0 1 2 3 4 5 Years After Baseline 0 0 1 2 3 4 5 Years After Baseline Runs a/o early VPC (202) Other complex VPC (260) Simple VPC only (433) No VPC (844) Ruberman W. Circulation. 1981;64(2):297-305.
Risk of SCD : Data from GISSI-2 Trial 1.00 0.98 1.00 0.98 p log-rank 0.0001 0.96 p log-rank 0.002 0.96 Survival 0.94 0.92 Survival 0.94 0.92 0.90 0.90 0.88 0.86 A 0 30 60 90 120 150 180 Days Patients without LV Dysfunction 0.88 B 0.86 0 30 60 90 120 150 180 No PVBs 1-10 PVBs/h > 10 PVBs/h Days Patients with LV Dysfunction Maggioni AP. Circulation. 1993;87:312
Significance of PVC Depends on the clinical setting Marker of Disease Severity Structural Heart Disease Myocardial infarction Congestive heart failure Underlying Cardiac Function
Management Patient with No Cardiac Disease Asymptomatic PVC No Treatment, regardless of configuration or frequency Reassurance Symptomatic PVC Elimination of causes Avoid substance(alcohol, tabocco, caffein ) Anxiolytics Beta-blocker, calcium channel blocker AADs(Class I and III) RFCA if highly symptomatic.
Management Patient with organic heart disease Depends on the clinical setting PVC suppression :efficacy not known(chf-stat, GESICA trial) Treatment of underlying condition Acute situation IV lidocaine, procainamide, propranolol and magnesium For long-term treatment AAD I, II including beta-blocker, and III(not Ic) RFCA ICD
Conclusion Management of PVC depends on the clinical setting PVC of normal heart, especially from RVOT, is always benign? Therefore, meticulous study for the assessment of clinical significance of PVC might be needed.