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Toronto Notes 2019 Ischemic Heart Disease
Indications
• paroxysmalSVT
■ AVNRT: accounts for more than half of all cases
• accessorypathway(orthodromicreciprocatingtachycardia):30%ofSVT
■ re-entrant rhythm, with an accessory AV connection as the retrograde limb ■ corrected by targeting the accessory pathway
• atrialflutter:re-entrypathwayinrightatrium
• AFib:potentialroleforpulmonaryveinablation
• ventriculartachycardia:focusarisesfromtherightventricularoutflowtractandlesscommonly
originates in the inferoseptal left ventricle near the apex (note: majority of cases of VT are due to scarring from previous MI and cannot be ablated)
Major Complications
• 1%ofpatients
• death: 0.1-0.2%
• cardiac: high grade AV block requiring permanent pacemaker (less risk with cryoablation), tamponade,
pericarditis
• vascular:hematoma,vascularinjury,thromboembolism,TIA/stroke • pulmonary: PE
Ischemic Heart Disease
Epidemiology
• mostcommoncauseofcardiovascularmorbidityandmortality
• Canadian-ledINTERHEARTstudyshowedthat9modifiableriskfactorsaccountedfor>90%ofMI • atherosclerosisandthrombosisarethemostimportantpathogeneticmechanisms
• M:F=2:1withallagegroupsincluded(Framinghamstudy),8:1forage<40,1:1forage>70
■ according to the Framingham Heart Study, men develop coronary heart disease at a rate double that of women for age <60; incidence in women triples shortly after menopause
• peakincidenceofsymptomaticIHDisage50-60(men)and60-70(women) • forprimarypreventionofischemicheartdiseaseseeFamilyMedicine,FM7
Table 7. Risk Factors and Markers for Atherosclerotic Heart Disease
Cardiology and Cardiac Surgery C25
Catheter Ablation for Atrial Fibrillation with Heart Failure (CASTLE-AF Trial)
NEJM 2018;378:417-427
Study: Multicenter, open-label, randomized, controlled trial
Population: 363patientswithsymptomatic paroxysmal or persistent AF; New York Heart Association class II, III, or IV HF; a left ventricular ejection fraction of ≤35 percent; failure or unwillingness to take antiarrhythmic drug therapy Intervention: catheter ablation vs. medical therapy Outcomes: primary endpoint was a composite of death from any cause or worsening of heart failure that led to an unplanned overnight hospitalization. Major secondary endpoints were death from
any cause, unplanned hospitalization related to heart failure, death from cardiovascular disease, cerebrovascular accident, unplanned hospitalization for cardiovascular disease, and any hospitalization. In the ablation group, procedure-related adverse events and atrial fibrillation-free intervals were
also assessed Results: After a median follow-up
of 37.8 months, the primary composite endpoint occurred in significantly fewer patients in the ablation group than in the medical-therapy group (28.5% vs. 44.6%; P=0.007). Significantly fewer patients in the ablation group died from any cause (13.4% vs. 25.0%; hazard ratio, 0.53; P=0.01), were hospitalized for worsening heart failure (20.7% vs. 66 35.9%; P=0.004), or died from cardiovascular causes (11.2% vs. 41 22.3%; P=0.009). Conclusions: Catheter ablation for atrial fibrillation in patients with heart failure was associated with
a significantly lower rate of a composite end point of death from any cause or hospitalization for worsening heart failure than was medical therapy.
Non-Modifiable Risk Factors
Age
Male, postmenopausal female Family history (FHx) of MI*
First degree male relative <55 First degree female relative <65
Modifiable Risk Factors
Hyperlipidemia* HTN*
DM*
Cigarette smoking* Psychosocial stress Obesity
Sedentary lifestyle Heavy alcohol intake
Smoking
Endothelial injury
Monocyte recruitment Enhanced LDL permeability
Markers of Disease
Elevated lipoprotein(a)
Hyperhomocysteinemia
Elevated high-sensitivity C-reactive protein (hsCRP) Coronary artery calcification
Carotid IMT/plaque
Ankle-brachial index
* Major risk factor Hypertension
Diabetes Mellitus
Dyslipidemia
Rheumatoid Arthritis
Monocytes enter into initial space and differentiate into macrophages – LDL is converted into oxidized-LDL (OX-LDL) Macrophages take up OX-LDL via scavenger receptors to become foam cells (’fatty streak’ and lipid core of plaque)
Cytokine and growth factor signaling from damaged endothelium and macrophages promote medial smooth muscle cell migration into the intima, proliferation (intimal hyperplasia), and release of matrix to form the fibrous cap of plaque – rupture depends on balance of pro- and anti-proteases, magnitude of necrosis and location of plaque (bifurcation sites are exposed to greater shear stress)
Calcification Plaque rupture Hemorrhage into plaque Fragmentation Wall weakening
Increased vessel wall rigidity Thrombosis Lumen narrowing Emboli Aneurysm
Figure 35. Pathophysiology of atherosclerosis