Info
🌱 來自: Huppert’s Notes
Ischemic Heart Disease🚧 施工中
Ischemic Heart Disease
Stable coronary artery disease (CAD)
• Types: Asymptomatic CAD or stable angina (angina that occurs reliably with exertion and emotional stress, relived with rest or nitroglycerin; due to fixed atherosclerosis)
• Diagnosis: Stress testing; computed tomography angiography (CCTA) vs. invasive coronary angiogram to assess anatomy
• Workup: HgA1c, lipid panel, ECG, TTE to assess LV function
• Treatment:
- Address risk factors and disease pathology:
• Smoking cessation
• Exercise/weight loss/diet
• Control hypertension (goal at least <140/90 mmHg), ACEi (or ARB if intolerant of ACEi)
• Treat DM (preferably with SGLT2 inhibitors or GLP-1 agonists)
• Treat HLD, start statin (e.g., atorvastatin, rosuvastatin; goal LDL <70 mg/dL)
- Consider addition of ezetimibe if LDL not at goal (IMPROVE-IT 2015)
- Consider addition of PCSK9 inhibitor if LDL still not at goal and/or family history (FOURIER 2018)
- Consider addition of icosapent ethyl if fasting triglycerides >135 mg/dL in patients with known CAD or DM (REDUCE-IT 2019)
• Aspirin (particularly if prior ACS event)
• Beta blocker (BB) (particularly if prior ACS event)
- Address symptoms (antianginal therapy for stable angina):
• Beta blocker (BB): Increases coronary blood supply (↓HR → ↑coronary diastolic filling time → ↑blood supply) and decreases myocardial demand (↓contractility → ↓wall stress/O2 demand)
• Calcium channel blocker (CCB): If second agent required; similar mechanism as BB
• Nitrates: Vasodilation of coronary arteries; venodilation → ↓preload → ↓wall stress/O2 demand
- Nitroglycerin (sublingual/transdermal/spray; taken as needed)
- Isosorbide dinitrate (oral; taken BID or TID)
- Isosorbide 5-mononitrate (oral; taken daily or BID)
• Ranolazine: Inhibits late inward sodium current in ischemic myocytes (Phase 0) → ↓Ca2+ overload → ↓wall stress/O2 demand and ↑coronary blood flow.
• Revascularization: Consider in patients who are symptomatic despite optimal medical therapy; only revascularize physiologically significant lesions as identified by stress testing or fractional flow reserve (FAME 2 2012; ISCHEMIA 2020).
- EXCEPTIONS: Revascularization has mortality benefit in:
• Significant left main disease (i.e., >50% stenosis LAD): All patients should be revascularized; CABG vs. PCI depends on anatomic complexity and surgical candidacy; decision should be made after multidisciplinary review.
• Significant 3-vessel CAD (i.e., >70% stenosis in 3 vessels): All patients should be revascularized; CABG preferred to PCI in patients who are good surgical candidates (SYNTAX 2009), especially in patients with diabetes (FREEDOM 2012).
• HFrEF: Consider revascularization, especially if severe CAD or viable myocardium (limited data, though may have long-term benefit).
Myocardial infarction
• Type I MI: Spontaneous MI (aka acute coronary syndrome from thrombus in a coronary artery) (Figure 1.13)
- ACS without ST elevation (NSTEMI)
• NSTEMI: Subendocardial ischemia
- Criteria: Rise and/or fall in troponin (Table 1.6) AND at least one of the following:
• Symptoms of acute myocardial ischemia
• New ischemic ECG changes (e.g., significant ST-T changes or LBBB)
• Development of pathologic Q waves
• Imaging evidence of loss of myocardial function (e.g., new wall motion abnormality)
• Coronary thrombus on angiography
• Unstable angina: Angina at rest without troponin elevation or ECG changes; concept was developed in the era before sensitive biomarkers; becoming less clinically relevant and not included in the current guideline definition of MI; however, patients with worsening anginal symptoms often merit expedited evaluation with stress testing or coronary angiogram.
- ACS with ST elevation (STEMI): Transmural ischemia
• Type II MI: MI due to ischemic imbalance (aka demand ischemia) (Figure 1.13)
FIGURE 1.13: Pathophysiology of type 1 and type 2 myocardial infarction.
- Frequent cause of elevated troponin in patients with hemodynamic stressors (e.g., sepsis, severe hypertension), especially in patients with underlying stable CAD.
- Treat the underlying hemodynamic cause.
• Coronary vasospasm:
- Etiology: Transient coronary vasospasm that causes angina at rest.
- Clinical: Classically chest pain that occurs at night in young women who smoke cigarettes and have migraines or Raynaud‘s; often co-occurs with CAD; can occur in patients on vasopressors.
- Diagnosis: ECG with transient ST elevation that occurs during an episode of chest pain. Can mimic STEMI. Provocation testing: Hyperventilation, intracoronary acetylcholine.
- Treatment: Smoking cessation, CCB, long-acting nitrate to prevent attacks, PRN nitrate to abolish attacks. Avoid nonselective beta blockers.
TABLE 1.6 • Troponins: Definition and Assays
Acute coronary syndrome (ACS)
• Diagnosis: Diagnosis should be suspected based on a combination of history, ECG, and troponin; confirmed by invasive coronary angiography
• Initial medical therapy:
- Aspirin (ASA): 325 mg PO ×1 chewed (VA Cooperative Study 1983; ISIS-2 1988), then 81 mg daily
- Anticoagulation: Enoxaparin 1 mg/kg SQ q12h has the strongest evidence (ESSENCE 1997; ExTRACT-TIMI 25 2006), although heparin gtt often used because fast on/off if going to the cath lab so it can be held for arterial access; ensure SBP <180 mmHg and DBP <110 mmHg prior to administration of the anticoagulant
- PGY12 inhibitor:
• Clopidogrel (Plavix): Load with 600 mg ×1, then 75 mg daily (CURE 2001). Consider decreasing load to 300 mg if age >75 yr. If a patient is already on Plavix, reload in the setting of an acute ACS event (ARMYDA-8 RELOAD-ACS 2013).
• Ticagrelor: Load with 180 mg PO ×1, then 90 mg PO BID (PLATO 2009 ticagrelor > clopidogrel; TREAT 2019 ticagrelor = clopidogrel)
• Prasugrel: Load with 60 mg PO ×1, then 10 mg PO daily (ISR-REACT5 2019 prasugrel > ticagrelor)
- Statin: Atorvastatin 80mg PO or rosuvastatin 40 mg PO, then daily (MIRACL 2001)
- Beta blocker: Metoprolol tartrate (or carvedilol if hypertensive) to goal HR<60 bpm. Hold in patients with hypotension, bradycardia, or if there is evidence of heart failure
- ACEi: Captopril or lisinopril if hypertensive and normal renal function
- Pain control:
• Sublingual nitroglycerin 0.4 mg q5min × 3, hold if SBP <100 mmHg, caution if RV infarct
• Nitroglycerin gtt (start in patients that are still having pain after they have been treated with SL nitro ×3)
• Ongoing chest pain indicates ongoing ischemia, so it is critical to use the above medications to try to get patients chest pain free. If chest pain cannot be resolved with medical management, then the patient should be taken to the cath lab urgently
• Avoid opioids due to increased mortality
• Revascularization: PCI as soon as possible; can administer fibrinolytics/tPA if PCI is unavailable
- STEMI: Indication for immediate revascularization; “door to balloon time” should be <90 min
- NSTEMI: Revascularization is important but not as urgent in most cases (see exceptions below); generally can be done within 24–48 hr
• Indications for immediate revascularization:
- Acute heart failure or cardiogenic shock
- Sustained ventricular arrhythmias
- Mechanical complications (e.g., acute MR, VSD)
- Refractory chest pain despite medication therapy
• Urgent (within 24 hours) catheterization if intermediate to high risk (e.g., TIMI >3)
Risk scores: 1) TIMI (Antman et al. 2000); 2) GRACE; 3) Killip. These scores can help determine the urgency of cardiac cath for NSTEMIs.
• Possible peri-MI complications:
- Pump failure: Flash pulmonary edema, heart failure, cardiogenic shock
- Thrombus and stroke (in setting of akinetic heart)
- Recurrent infarction (hours–days)
- Arrhythmias: Ischemic VT/VF
- Mechanical complications:
• Free wall rupture (hours–2 weeks): Pericardial tamponade with sudden hypotension, distant heart sounds; can cause PEA arrest and death
• Interventricular septal rupture (hours–2 weeks): New VSD with holosystolic murmur with thrill, hypotension, respiratory distress
• Papillary muscle rupture (2 days to 1 week): New MR with holosystolic murmur that radiates to the axilla, pulmonary edema, respiratory distress
• Ventricular aneurysm: (weeks–months): ECG demonstrates persistent ST elevation; risk of clot/embolism, arrhythmias, angina, heart failure
- Pericarditis:
• Post-infarction pericarditis ([PIP], within days): Pleuritic, positional. Diffuse ST elevations, PR depressions. Treatment: Pain relief; continue ASA
• Post-cardiac injury syndrome ([PCIS], also called Dressler’s, weeks–months): Pericarditis due to an immune reaction; positional chest pain, friction rub, fever. Treatment: ASA +/- colchicine
• Post-MI management:
- Aspirin 81 mg PO daily for life
- Atorvastatin 80 mg PO daily for life (or another high-intensity statin); LDL goal <70 mg/dL (can add ezetimibe, PCSK9 inhibitor as needed)
- PGY12 inhibitor (clopidogrel, ticagrelor, or prasugrel) for 1 yr post-MI (maybe longer if high ischemic risk and low bleeding risk)
- Beta blocker
- ACEi/ARB
- Spironolactone/eplerenone if EF <40% and either DM or heart failure symptoms
- TTE to assess LV function
- Lifestyle modification: Smoking cessation, weight loss, exercise, diet
- Diabetes control (ideally with SGLT2 inhibitors or GLP1 agonists)
- Cardiac rehabilitation
- Implantable cardioverter-defibrillator (ICD): Indicated if post-MI EF<35% despite medical therapy ×40 days or sustained VT/VF >2 days post-MI not due to reversible ischemia