What process describes the progressive thinning and dilation of infarcted myocardium that contributes to worsening heart failure?
Ventricular remodeling
Below what ejection fraction is systolic dysfunction in ischemic cardiomyopathy typically considered severe?
Less than 35 percent
What heart-failure medication class blocks both angiotensin II and neprilysin to improve mortality and reverse remodeling?
ARNIs (angiotensin-receptor–neprilysin inhibitors)
ex. Sacubitril/valsartan (Entresto)
What pulmonary-capillary wedge pressure threshold indicates elevated left-sided filling pressures?
> 15 mm Hg
What arrhythmia accounts for most sudden deaths in ischemic cardiomyopathy?
Ventricular tachyarrhythmia (VT or VF)
Which neurohormonal system (activated after myocardial infarction) promotes fibrosis and adverse remodeling?
The renin–angiotensin–aldosterone system (RAAS)
What biphasic response on dobutamine stress echo indicates viable but jeopardized myocardium?
Improved contraction at low dose, worsening at high dose
Which SGLT2 inhibitor first showed mortality benefit in HFrEF independent of diabetes?
Dapagliflozin
Which imaging technique uses FDG uptake to assess metabolic viability of myocardium?
Cardiac PET
Severe LV dysfunction (< 30 %) predisposes to formation of what intracardiac complication?
LV apical thrombus
What term refers to reversible myocardial dysfunction that persists after transient ischemia, despite restored perfusion?
Myocardial stunning
On cardiac MRI, what percentage of transmural late gadolinium enhancement predicts non-viable (scarred) myocardium?
Greater than 50 percent of wall thickness
What landmark trial demonstrated a survival benefit of CABG in patients with ischemic cardiomyopathy and low EF?
The STICH trial
A Qp:Qs ratio greater than 1.0 after infarction suggests what mechanical complication?
Left-to-right shunt from a ventricular septal defect
The Seattle Heart Failure Model incorporates this biomarker to estimate prognosis
BNP or NT-proBNP
How does the fibrosis pattern differ between ischemic and non-ischemic (idiopathic) dilated cardiomyopathy?
Ischemic: patchy fibrosis following coronary distribution
Non-ischemic: diffuse interstitial fibrosis
DOUBLE JEOPARDY
According to the STICH and REVIVED-BCIS2 data, what specific subgroup of patients with ischemic cardiomyopathy demonstrates clear survival benefit from CABG over medical therapy alone, and why?
Patients with extensive multivessel or left main coronary artery disease and viable myocardium, because CABG reduces future ischemic burden and malignant arrhythmia risk even when EF remains low.
The benefit arises from reduction in sudden cardiac death and recurrent ischemia, not necessarily from improvement in EF
ICD implantation is indicated for primary prevention of sudden death if EF ≤ 35 % after how long on optimal therapy?
At least three months
What pattern of strain reduction on echocardiography distinguishes ischemic from non-ischemic cardiomyopathy?
Regional strain reduction corresponding to coronary territories
What post-infarction structural change predicts higher mortality and arrhythmic risk on echo?
Left-ventricular aneurysm
Which myocardial layers are most vulnerable to chronic subendocardial ischemia?
Subendocardial and mid-myocardial layers
Chronic anterior-wall infarction often produces what classic ECG finding?
Deep Q waves in V1–V4 with poor R-wave progression
What are the standard ECG and mechanical criteria for CRT eligibility in ischemic cardiomyopathy?
LVEF ≤ 35 %, sinus rhythm, and QRS ≥ 150 ms with LBBB morphology
On cardiac MRI, what distribution of enhancement signifies ischemic injury versus non-ischemic?
Subendocardial or transmural enhancement following coronary territories
DOUBLE JEOPARDY
In chronic ischemic cardiomyopathy, persistent subendocardial hypoperfusion leads to selective downregulation of this sarcoplasmic reticulum calcium-handling protein, resulting in impaired lusitropy and contractility.
SERCA2a (sarcoplasmic/endoplasmic reticulum Ca²⁺-ATPase 2a)
Its dysfunction contributes to abnormal calcium reuptake, delayed relaxation, and diastolic dysfunction --> a therapeutic target for gene therapy trials.