In a patient with reduced end‑diastolic volume relative to stroke volume, grade 1 diastolic dysfunction without overt diastolic heart failure, and a calcified left anterior descending artery, how likely is systemic vascular resistance from the calcified artery to be causing a decrease in preload?

Systemic Vascular Resistance from Calcified LAD is Extremely Unlikely to Reduce Preload

A calcified LAD (coronary artery) does not contribute to systemic vascular resistance (SVR) and therefore cannot reduce preload. This represents a fundamental misunderstanding of cardiovascular physiology that needs immediate clarification.

Why This Mechanism is Physiologically Impossible

Coronary Arteries Do Not Contribute to SVR

• SVR is determined by resistance in systemic arterioles (precapillary resistance vessels), not epicardial coronary arteries 1, 2
• The calcified LAD is a large epicardial coronary artery that supplies myocardial perfusion—it is not part of the systemic arterial circulation that determines afterload 1
• Even complete occlusion of the LAD would cause myocardial ischemia/infarction, not increased SVR 1

The Actual Relationship Between SVR and Preload

• Increased SVR (true systemic afterload) does not reduce preload—it reduces stroke volume by increasing left ventricular afterload 1
• When afterload increases, the ventricle must generate higher wall stress to eject blood, which can reduce stroke volume and increase end-systolic volume 1
• Preload (end-diastolic volume) is determined by venous return, ventricular compliance, and filling time—not by arterial resistance 2, 3

What is Actually Causing Your Patient's Reduced EDV/SV

Grade 1 Diastolic Dysfunction Explains the Findings

• In diastolic dysfunction, impaired ventricular relaxation and reduced compliance limit EDV despite adequate filling pressure 1
• The ventricle operates on a steeper portion of its pressure-volume curve, meaning small increases in volume cause disproportionate increases in filling pressure 1
• This patient likely has exhausted preload reserve—the ventricle cannot accommodate additional volume even if venous return increases 2, 3

Reduced EDV Reflects Impaired Filling, Not Reduced Venous Return

• Preload reserve is the difference between current EDV and maximal possible EDV 3
• In diastolic dysfunction, even "normal" filling pressures may represent near-maximal EDV due to chamber stiffness 2, 4
• The reduced EDV/SV pattern suggests the ventricle is operating near its limited volumetric capacity 3, 5

The Calcified LAD's Actual Clinical Significance

What the LAD Calcification Actually Threatens

• Calcified coronary arteries indicate atherosclerotic disease that can cause myocardial ischemia, reducing contractility and worsening both systolic and diastolic function 1
• Subendocardial ischemia from flow-limiting LAD stenosis would impair diastolic relaxation, further limiting EDV 1
• This creates a vicious cycle: reduced coronary perfusion → impaired relaxation → reduced EDV → reduced stroke volume → reduced cardiac output 1

Distinguishing Ischemic from Non-Ischemic Causes

• Assess for anginal symptoms, regional wall motion abnormalities on echo, and consider stress testing or coronary angiography 1
• If the LAD stenosis is hemodynamically significant, revascularization could improve diastolic function by restoring myocardial perfusion 1

Common Pitfall to Avoid

• Do not confuse coronary artery disease (which affects myocardial perfusion and contractility) with systemic vascular resistance (which is determined by peripheral arterioles) 1, 2
• The calcified LAD threatens myocardial oxygen supply, not systemic hemodynamics 1
• Central venous pressure and pulmonary capillary wedge pressure are insensitive indicators of preload status—echocardiographic EDV measurement provides direct assessment 2, 3