How to Interpret Cardiac Catheterization Findings

Introduction

The catheterization report arrives dense with numbers, anatomical descriptions, and categorical assessments that determine your treatment path. A stenosis percentage that crosses certain thresholds triggers stent consideration. An FFR value on one side of 0.80 or the other shifts management entirely. Understanding what these numbers mean—and what they do not mean—allows more informed participation in decisions about your care.

The interpretation challenge extends beyond technical understanding to fundamental questions about what catheterization actually measures. An angiogram shows anatomy, but heart attacks occur based on biology—plaque rupture, thrombosis, inflammation. A 40% blockage made of vulnerable plaque may pose greater immediate danger than a stable 80% stenosis. These nuances rarely make it into the simplified stenosis percentages that dominate clinical conversations.

This article explains how to read catheterization findings, understand the terminology, and recognize the limitations of the information. Subsequent articles address what the clinical evidence shows about acting on these findings and how to navigate treatment decisions when faced with results that could support multiple approaches.

What does “percent stenosis” mean and how is it measured?

Percent stenosis quantifies how much a coronary artery’s diameter has narrowed at its tightest point compared to adjacent “normal” segments. A 70% stenosis means the diameter at the narrowest point is 70% smaller than the reference diameter—or equivalently, only 30% of the original diameter remains. This simple fraction drives most clinical decision-making despite its substantial limitations.

Measurement occurs through visual estimation or quantitative analysis. In visual estimation, the cardiologist eyeballs the angiogram and estimates the narrowing percentage. This approach is fast but subjective. Quantitative coronary angiography (QCA) uses software to measure vessel edges and calculate stenosis mathematically, improving reproducibility but not addressing fundamental limitations of anatomical assessment.

The reference segment selection critically influences the result. If the cardiologist chooses a segment that is itself diseased as the reference, the apparent stenosis appears less severe than if a truly normal segment were used. Diffusely diseased arteries may show no focal stenosis despite harboring extensive atherosclerosis. The angiogram sees only the lumen silhouette, missing disease that has remodeled outward into the vessel wall.

Why might different cardiologists estimate different blockage percentages from the same images?

Interobserver variability in angiographic interpretation is well-documented and substantial. Studies comparing experienced cardiologists reviewing identical angiograms show disagreements of 10-20% in stenosis estimates. A lesion one cardiologist calls 60% might be labeled 75% by another—a difference that could change treatment recommendations.

Several factors drive this variability. The angiogram displays a three-dimensional structure in two dimensions, and vessel curvature creates foreshortening that distorts apparent severity. Viewing angle selection affects which portion of an eccentric stenosis is visualized. Contrast streaming patterns can suggest narrowing where disease is minimal or obscure true stenoses.

Reference segment selection adds another layer of subjectivity. Deciding what constitutes “normal” in a diffusely diseased artery requires judgment. The same narrowing appears more or less severe depending on the chosen comparator. Some cardiologists apply consistent criteria; others adjust based on clinical context in ways that may introduce bias toward intervention.

What is the difference between anatomically significant and functionally significant blockages?

Anatomical significance refers to the degree of luminal narrowing visible on angiography. By convention, stenoses of 70% or greater in epicardial coronary arteries (or 50% in the left main) are considered anatomically significant. These thresholds derive from older studies correlating angiographic severity with abnormal stress test results, not from evidence that intervention improves outcomes.

Functional significance refers to whether a stenosis actually impairs blood flow to the myocardium. Fractional flow reserve measurement directly assesses this by comparing pressure proximal and distal to a lesion during maximal hyperemia (Tonino et al., 2009). FFR ≤0.80 indicates the lesion limits flow and would benefit from revascularization; FFR >0.80 indicates adequate flow despite the anatomical appearance.

The discordance between anatomy and function is clinically common. Studies show that approximately 20% of lesions appearing severe on angiography are not functionally significant, while some moderate-appearing lesions are flow-limiting. The FAME 2 trial demonstrated that FFR-guided decision-making reduces unnecessary intervention while identifying patients who benefit (De Bruyne et al., 2012). This physiological approach challenges the traditional anatomy-first paradigm.

What does an FFR value mean and what threshold indicates a significant blockage?

FFR represents the ratio of maximum achievable blood flow through a stenotic artery to maximum flow if the artery were completely normal. An FFR of 0.80 means the stenosis permits only 80% of normal maximum flow—a 20% reduction. An FFR of 0.70 indicates 30% reduction. An FFR of 1.0 would indicate no flow limitation.

The threshold of FFR ≤0.80 for functional significance emerged from validation studies correlating FFR values with non-invasive ischemia testing and clinical outcomes. The FAME trial established that deferring intervention when FFR >0.80 is safe, with outcomes comparable to or better than stenting such lesions (Tonino et al., 2009). Lesions with FFR ≤0.80 show improved outcomes with revascularization compared to medical therapy alone in most studies.

The threshold should not be interpreted with rigid precision. FFR is a continuous variable—a lesion with FFR 0.79 differs trivially from one at 0.81 despite falling on opposite sides of the cutoff. Clinical judgment should integrate FFR with other factors including symptoms, anatomy, and patient preferences. Some specialists use a “gray zone” of 0.75-0.80 where additional information guides decisions.

How do catheterization findings correlate with symptoms?

The relationship between angiographic findings and symptoms is weaker than many patients expect. Substantial coronary artery disease can exist without symptoms, particularly in patients with diabetes or peripheral neuropathy who may have impaired pain sensation. Conversely, patients with minimal or no coronary disease sometimes experience typical anginal symptoms from other causes.

Studies of patients with stable angina and documented ischemia show that neither angiographic severity nor ischemia extent reliably predicts symptom burden or response to treatment (Reynolds et al., 2021). The ISCHEMIA trial found that patients with severe ischemia did not consistently have more symptoms than those with moderate ischemia, and symptom improvement occurred with both invasive and conservative strategies.

Several factors explain this disconnect. Collateral vessels can compensate for blockages, maintaining perfusion despite severe stenosis. Ischemic preconditioning may reduce pain perception. Symptom reporting is subjective and influenced by expectations, anxiety, and comorbidities. A clean angiogram does not rule out cardiac causes of chest pain, particularly microvascular disease that angiography cannot visualize.

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What does “normal coronary arteries” on catheterization actually mean?

A report of “normal coronary arteries” means the angiogram shows no significant luminal narrowing—typically defined as all stenoses less than 50%. This is reassuring regarding obstructive coronary disease but does not mean the arteries are completely free of atherosclerosis or that the heart is entirely healthy.

Angiography visualizes only the lumen. Early atherosclerosis that has remodeled outward into the vessel wall—so-called positive remodeling—remains invisible on angiograms. Intravascular ultrasound studies of angiographically normal segments frequently reveal substantial plaque burden hidden within the vessel wall (Calvert et al., 2011). A patient told their arteries are “clean” may harbor significant atherosclerosis undetected by angiography.

Non-obstructive coronary artery disease—visible plaque that does not meet significance thresholds—carries prognostic implications that were historically underappreciated. Patients with angiographic disease of any severity have higher cardiovascular risk than those with truly normal arteries. Additionally, normal coronary arteries do not explain anginal symptoms, which may indicate microvascular dysfunction, coronary spasm, or non-cardiac causes requiring further evaluation.

What is coronary microvascular disease and can catheterization detect it?

Coronary microvascular disease (CMD) affects the small vessels that penetrate into the heart muscle, beyond the epicardial arteries visible on angiography. These vessels regulate blood flow at the tissue level. When dysfunctional, they produce ischemia and symptoms despite normal-appearing epicardial arteries—a condition increasingly recognized as clinically significant.

Standard angiography cannot directly visualize microvessels. However, catheterization can assess microvascular function indirectly. Coronary flow reserve (CFR) measurement during catheterization evaluates the ability of the coronary circulation to increase flow in response to demand (Rahman et al., 2021). Impaired CFR with normal epicardial arteries suggests microvascular disease. The index of microvascular resistance (IMR) provides another catheter-based assessment.

Recognition of CMD has grown substantially. Studies suggest it affects a substantial proportion of patients with angina and non-obstructive coronary disease, particularly women. Diagnosis requires moving beyond the binary of “significant stenosis” versus “normal arteries” to consider physiological function. Treatment approaches differ from obstructive disease, emphasizing medications that improve microvascular function rather than revascularization.

What does the catheterization report terminology mean?

Catheterization reports use standardized anatomical nomenclature. The left main coronary artery divides into the left anterior descending (LAD) and left circumflex (LCx) arteries. The right coronary artery (RCA) is the third major vessel. Each has named branches—the LAD gives off diagonals and septal perforators; the LCx supplies obtuse marginals; the RCA provides posterior descending and posterolateral branches.

Descriptive terms characterize stenoses. “Mild” typically means less than 50%, “moderate” indicates 50-69%, and “severe” means 70% or greater. “Diffuse” describes disease spread along the artery length rather than focal narrowing. “Calcified” indicates visible calcium in the plaque. “Eccentric” describes stenoses that narrow the lumen asymmetrically.

Dominance describes which artery supplies the posterior descending artery (PDA). Right dominance (most common) means the RCA supplies the PDA. Left dominance means the LCx supplies it. Codominance indicates shared supply. Dominance affects the significance of disease in each vessel—disease in a dominant RCA affects more myocardium than disease in a non-dominant RCA.

How does plaque location affect the significance of findings?

Proximal lesions generally carry greater significance than distal lesions because they jeopardize more downstream myocardium. A proximal LAD stenosis affects blood supply to the anterior wall, septum, and apex—a large territory. A distal LAD stenosis affects only the apex. The same stenosis percentage has different implications depending on location.

The left main coronary artery deserves special attention because it supplies most of the left ventricle. Left main stenosis threatens the largest myocardial territory of any single lesion. Guidelines use a lower threshold (50%) for significance compared to other vessels (70%), and left main disease often prompts consideration of bypass surgery rather than stenting (Ong et al., 2006).

Bifurcation lesions—stenoses at branch points—present technical challenges and historically worse outcomes with intervention. A stenosis involving the LAD and a major diagonal differs from a stenosis involving only the mid-LAD. Ostial lesions at artery origins create specific challenges for both assessment and treatment. These anatomical factors influence treatment planning beyond simple stenosis percentages.

What is left main disease and why is it particularly important?

The left main coronary artery is a short trunk that supplies blood to the left anterior descending and left circumflex arteries before branching. Significant left main stenosis therefore jeopardizes the majority of left ventricular blood supply. Acute left main occlusion is typically fatal due to massive infarction.

Left main disease has traditionally indicated bypass surgery rather than percutaneous intervention. The protection afforded by multiple bypass grafts was considered superior to stenting a single critical location. More recent trials comparing PCI to CABG for left main disease show comparable outcomes in selected patients, though long-term data still favor surgery in complex anatomy (Mrevlje, 2024).

Assessment of left main disease requires particular care. The ostium of the left main is challenging to image because standard catheter engagement obscures it. IVUS is particularly valuable for left main assessment, providing accurate measurement of true vessel dimensions and disease extent (Hong et al., 2015). Underestimating left main disease can lead to inadequate treatment; overestimating it can prompt unnecessary surgery.

What are collateral vessels and what does their presence indicate?

Collateral vessels are natural bypass channels that develop when chronic coronary obstruction stimulates new vessel growth. Blood finds alternative routes to supply myocardium beyond the blockage. Well-developed collaterals can maintain adequate perfusion despite complete coronary occlusion, sometimes allowing patients to tolerate total blockage without infarction.

The presence of collaterals indicates chronic rather than acute disease. Collateral development takes time—weeks to months. Their visibility on angiography suggests the obstruction has been present long enough for adaptive remodeling. Extensive collateral networks often accompany chronic total occlusions that have been present for years.

Collateral status affects intervention decisions. Good collaterals may protect against complications during intervention—if a vessel dissects or occludes during stent placement, collaterals can maintain some perfusion. However, collaterals do not eliminate the benefit of revascularization; restoring antegrade flow typically improves symptoms and function beyond what collaterals alone achieve (Panuccio et al., 2023). Chronic total occlusion intervention is a subspecialty field focused on these complex cases.

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How do catheterization findings relate to future heart attack risk?

The relationship between angiographic findings and heart attack risk is less straightforward than patients often assume. Heart attacks typically occur when vulnerable plaques rupture and trigger acute thrombosis. Vulnerable plaques are characterized by large lipid cores, thin fibrous caps, and inflammation—features invisible on standard angiography.

Stenosis severity does not reliably predict which lesions will cause future events. Studies following patients after catheterization found that heart attacks often arose from lesions that were not the most severe at baseline. The PROSPECT study using intravascular imaging identified plaque characteristics associated with future events—large plaque burden, small lumen area, and thin-cap fibroatheroma morphology—but even these markers had limited predictive power (Calvert et al., 2011).

This disconnect has profound implications. Fixing the “culprit” lesion that appears worst on angiography does not eliminate risk from other vulnerable plaques throughout the coronary tree. Medical therapy addressing systemic atherosclerosis—lipid lowering, anti-inflammatory treatment, antithrombotic therapy—may prevent events that intervention cannot. The catheterization report snapshots anatomy at a moment in time but does not reveal the dynamic biology driving disease progression.

What findings might lead to immediate intervention versus medical management?

Certain findings prompt immediate intervention without extensive deliberation. Acute myocardial infarction with a visible culprit lesion warrants emergent revascularization—the benefit is clear and time-critical. Left main stenosis or three-vessel disease with reduced heart function generally indicates revascularization given the survival benefit demonstrated in trials.

Stable findings in stable patients allow more measured decision-making. The ISCHEMIA trial enrolled patients with moderate to severe ischemia and stable coronary disease, finding no survival benefit from routine invasive management over medical therapy (Reynolds et al., 2021). Even severe stenosis in a patient without symptoms or ischemia might reasonably be managed medically, particularly if FFR shows adequate flow.

Between these extremes lies a broad gray zone where reasonable clinicians disagree. A symptomatic patient with a 70% proximal LAD stenosis and FFR of 0.78 could appropriately receive either stenting or intensified medical therapy. The “right” answer depends on patient preferences, symptom burden, life expectancy, and nuanced anatomical factors. Understanding that options exist—rather than viewing catheterization findings as mandating specific treatments—empowers more meaningful shared decision-making.

How should I interpret catheterization results if they differ from my CT angiogram?

CT angiography and invasive catheterization assess the same anatomy using different technologies, and discordance occurs. CT may overestimate stenosis severity due to calcium blooming artifacts or underestimate it due to motion artifact. Catheterization provides higher spatial resolution and multiple viewing angles but involves subjective interpretation.

When results conflict, context matters. CT angiography performs well for excluding significant disease—a clearly normal CT reliably predicts a normal catheterization. CT less reliably grades stenosis severity, particularly in calcified vessels where blooming artifact exaggerates narrowing. If CT showed concerning findings that prompted catheterization but the cath appears less severe, the catheterization finding generally takes precedence.

However, catheterization has its own limitations. Eccentric plaques may appear differently depending on imaging angle. Diffuse disease without focal stenosis can be underestimated. IVUS frequently reveals more extensive disease than angiography alone suggests (de Jaegere et al., 1998). When clinical suspicion remains high despite reassuring angiography, intravascular imaging or functional assessment may resolve the discrepancy.

What are common misunderstandings patients have about catheterization findings?

Patients often interpret stenosis percentages as precise measurements when they are estimates with substantial uncertainty. Being told you have a “70% blockage” sounds definitive, but the true value might be anywhere from 55% to 85% depending on who reads the images and how. This precision illusion drives treatment decisions that might differ with more accurate assessment.

Another common misunderstanding equates stenosis severity with heart attack risk. Patients assume their most severe blockage is the most dangerous, but vulnerable plaques causing acute events often arise from less severe lesions. The 40% lesion that appears innocent may pose greater immediate danger than the 70% stable lesion that prompted catheterization.

Finally, patients often believe that finding and fixing blockages provides definitive treatment of their coronary disease. Stenting addresses focal anatomy but does not cure atherosclerosis or eliminate risk from the unstented coronary tree. Medical therapy remains essential regardless of whether intervention occurs (Boden et al., 2007). The catheterization provides a snapshot, not a cure.

Conclusion

Catheterization findings require interpretation beyond face-value acceptance of stenosis percentages. Understanding the limitations of anatomical assessment, the variability in interpretation, and the disconnect between anatomy and outcomes positions patients to engage more meaningfully in treatment discussions.

The key questions to ask after catheterization are not just “how bad is the blockage?” but “does this blockage actually limit blood flow?”, “what does this mean for my prognosis?”, and “would fixing this improve my outcomes or just the anatomy?” The next articles address the clinical evidence for catheterization-guided intervention and how to navigate the decision-making process.