What are the recommendations for an adult male patient with an EKG (electrocardiogram) report showing sinus rhythm, borderline left axis deviation, abnormal Q wave progression, early transition, and borderline T wave abnormalities in the inferior leads?

Management of EKG Findings in Adult Male with Borderline Abnormalities

This constellation of borderline EKG findings—left axis deviation, abnormal R-wave progression with early transition, and inferior T-wave abnormalities—requires cardiac evaluation with echocardiography and comparison to prior EKGs, as these patterns may represent early markers of structural heart disease or coronary artery disease, particularly given the patient's male gender and adult age. 1, 2, 3

Immediate Clinical Assessment

Risk Stratification Based on Symptoms

• If the patient has chest pain, dyspnea, or syncope: Treat as potential acute coronary syndrome with immediate emergency department evaluation, 12-lead EKG, cardiac biomarkers (troponin), and risk stratification within 10 minutes 3
• If asymptomatic: Proceed with systematic outpatient evaluation, though the combination of findings warrants timely assessment rather than routine follow-up 1

Compare with Prior EKGs

• Obtain all available prior EKGs to determine if these findings are new or longstanding 2, 3
• New T-wave abnormalities carry significantly higher concern than chronic stable patterns 4, 5
• Technical factors like lead misplacement can cause spurious R-wave transition abnormalities and should be excluded by repeat EKG if findings are isolated 2, 6

Significance of Individual EKG Abnormalities

Borderline Left Axis Deviation

• Left axis deviation between -30° and -45° is considered moderate and may indicate left anterior fascicular block, which often reflects underlying structural heart disease 1, 7
• In athletes, isolated left axis deviation without other abnormalities may not require investigation if family history is negative 1
• However, when combined with other EKG abnormalities (as in this case), it increases concern for pathology 1

Abnormal R-Wave Progression and Early Transition

• Early transition (R>S before V3) combined with poor R-wave progression constitutes a high-risk pattern highly indicative of cardiac disease, particularly left anterior descending coronary artery stenosis 2, 3
• This pattern may also indicate prior anterior myocardial infarction, even in the absence of clinical history 2
• In a 75-year-old male with alcohol use, these findings carry higher concern due to increased coronary artery disease risk 2

Borderline T-Wave Abnormalities in Inferior Leads

• T-wave abnormalities ≥1 mm (0.1 mV) in depth in leads with dominant R waves (including inferior leads II, III, aVF) are considered abnormal and warrant investigation 1, 3
• T-wave abnormalities predict development of major Q-wave patterns with odds ratio 3.11, and 63% of patients developing Q-waves had no prior MI hospitalization 5
• Even borderline T-wave changes independently predict cardiovascular morbidity and sudden cardiac death risk 8, 5

Mandatory Diagnostic Workup

Transthoracic Echocardiography (First-Line)

• Essential to assess: left ventricular wall motion abnormalities, regional wall motion suggesting prior infarction, left ventricular hypertrophy, chamber dimensions, and ejection fraction 2, 3
• Echocardiography can distinguish physiologic from pathologic left ventricular hypertrophy 1
• 26 of 29 patients with new ST-T abnormalities had left ventricular hypertrophy on echocardiography 4

Cardiac Biomarkers

• Measure troponin to exclude acute myocardial infarction, particularly if any symptoms present 2, 9

Additional Testing Based on Initial Results

• If echocardiography shows regional wall motion abnormalities: Coronary angiography or stress testing with imaging to assess for coronary artery disease 2
• If echocardiography is non-diagnostic but clinical suspicion remains high: Cardiac MRI with gadolinium to detect subtle myocardial fibrosis, assess for cardiomyopathy phenotypes, and evaluate both right and left ventricular involvement 3, 9
• If intermediate pre-test probability for coronary artery disease: Stress testing with imaging 2

Critical Pitfalls to Avoid

Do Not Dismiss as "Nonspecific" Without Investigation

• The term "borderline" does not mean benign—these findings require evaluation 1, 3
• T-wave abnormalities may represent the only sign of inherited cardiomyopathy before structural changes become evident 1, 3
• Abnormal EKG repolarization may identify subjects at risk for subsequent development of structural heart disease that may not be evident until years later 1

Do Not Assume Normal Initial Imaging Excludes Disease

• Athletes with repolarization abnormalities should have imaging studies on a regular (annual) basis even when initial comprehensive imaging is normal 1
• Genotype-phenotype studies reveal EKG abnormalities may be the only sign of disease in mutation carriers before morphologic changes appear 1

Consider Age-Specific Context

• In adults ≥60 years, even slight T-wave negativity (<1 mm) in lateral leads occurs in only 2-5% of the population, making most T-wave abnormalities pathologic in elderly patients 3
• Blood pressure gradually increases over 10 years before ST-T abnormalities develop (127/78 to 144/84 mmHg), emphasizing the importance of longitudinal risk factor assessment 4

Ongoing Surveillance

If Initial Workup is Normal

• Serial EKGs and cardiac imaging are necessary to monitor for development of cardiomyopathy phenotype 9
• Annual echocardiography is usually sufficient, but use other imaging modalities when images are suboptimal 1
• Continue clinical surveillance with attention to development of symptoms 1, 3

Address Modifiable Risk Factors

• Assess and manage hypertension, as blood pressure elevation precedes ST-T abnormality development 4
• Evaluate lipid profile including lipoprotein(a), which predicts Q-wave development 5
• Screen for diabetes, as high fasting glucose predicts ST-segment depression 5
• If alcohol use is present, provide appropriate counseling as chronic alcohol use is associated with cardiomyopathy 2