Demand Ischemia Causes and Management

Primary Causes of Demand Ischemia

Tachycardia/tachyarrhythmias increase myocardial workload, reducing diastolic filling time and increasing oxygen demand, according to the American Heart Association 1, 2
Hypertension elevates left ventricular afterload and myocardial work, as stated by the American College of Cardiology 3, 4
Left ventricular hypertrophy increases myocardial mass and oxygen requirements, as noted by the American College of Radiology 5, 6
Aortic valve stenosis creates pressure overload and increased ventricular wall stress, as reported by the American Heart Association 4
Hypertrophic cardiomyopathy increases myocardial mass and oxygen consumption, according to the American College of Cardiology 4
Fever elevates metabolic rate and cardiac output requirements, as stated by the American Heart Association 4
Hyperthyroidism increases heart rate and contractility, as noted by the American College of Cardiology 4
Arteriovenous fistula increases cardiac output demands, as reported by the American Heart Association 4

Hypoxemia decreases arterial oxygen content, as stated by the American College of Cardiology 4
Hypotension reduces coronary perfusion pressure, according to the American Heart Association 1, 4
Coronary microvascular dysfunction impairs myocardial perfusion despite patent epicardial vessels, as noted by the American College of Cardiology 5
Elevated ventricular filling pressures reduce the coronary perfusion gradient, as reported by the American Heart Association 1
Coronary vasospasm transiently reduces coronary blood flow, according to the American College of Radiology 6

Demand ischemia develops through a "perfect storm" of conditions that create an imbalance between oxygen supply and demand, as stated by the American Heart Association 1
Coronary blood flow may be compromised by low cardiac output or reduced diastolic blood pressure, according to the American College of Cardiology 1
Elevated ventricular filling pressures worsen the situation by reducing the driving gradient for coronary perfusion, as noted by the American Heart Association 1
Oxygen demand simultaneously increases due to elevated ventricular wall stress and neurohormone-mediated increases in heart rate and contractility, as reported by the American College of Cardiology 1

Troponin elevation occurs due to myocyte injury even without epicardial coronary artery occlusion, as stated by the American College of Cardiology 1, 7
ECG changes may show ST-segment depression or T-wave inversions rather than ST elevation, according to the American Heart Association 7, 2
Symptoms may include chest discomfort, dyspnea, fatigue, or be asymptomatic, as noted by the American College of Cardiology 7

Sepsis combines tachycardia, hypotension, and increased metabolic demands, as reported by the American College of Cardiology 2
Gastrointestinal bleeding causes anemia and often tachycardia, according to the American Heart Association 4
Acute exacerbation of COPD combines hypoxemia with increased work of breathing, as stated by the American College of Cardiology 4
Severe aortic stenosis creates pressure overload with limited ability to increase coronary flow, as noted by the American College of Radiology 6, 4

Elevated cardiac biomarkers (troponin) may be present despite absence of acute coronary plaque rupture, as reported by the American College of Cardiology 1, 7
A rising and/or falling pattern of troponin is still important to distinguish acute from chronic elevations, according to the American Heart Association 7
Evaluation should focus on identifying both the underlying cause of the supply-demand imbalance and any contributing coronary disease, as stated by the American College of Cardiology 2, 4

Address the underlying cause of increased demand or decreased supply, as reported by the American Heart Association 4
Optimize hemodynamics (control heart rate, maintain adequate blood pressure), according to the American College of Cardiology 3
Consider beta-blockers to reduce myocardial oxygen consumption in appropriate patients, as stated by the American Heart Association 3, 4
Treat underlying coronary disease if present, as noted by the American College of Cardiology 2, 6

The American College of Cardiology/American Heart Association defines Type 2 myocardial infarction as a demand-supply mismatch, which occurs when conditions other than coronary artery disease contribute to an imbalance between myocardial oxygen supply and/or demand, including scenarios involving tachyarrhythmias, coronary endothelial dysfunction, coronary artery spasm, anemia, respiratory failure, and hypotension 8

Rate-related ischemia presents with distinct characteristics, including troponin elevation despite absence of acute coronary plaque rupture, reflecting myocyte injury from supply-demand mismatch, and ECG changes typically show ST-segment depression or T-wave inversions rather than ST elevation 8

The key distinction from Type 1 MI is the absence of acute atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with intraluminal thrombus, and demand ischemia can unmask underlying coronary disease, so evaluation must address both the precipitating cause and any contributing coronary pathology 8