Diagnosing HFpEF relies on demonstrating elevated left-sided filling pressures during exertion, because symptoms typically appear with activity even when the ejection fraction is preserved. The most definitive way to prove this is through invasive hemodynamic testing during exercise: right heart catheterization with supine bicycling and simultaneous VO2 monitoring to measure the pulmonary capillary wedge pressure as the patient exercises. This directly shows how filling pressures rise with increased demand, which is the hallmark of HFpEF. Resting measurements can miss the problem, since filling pressures may be normal at rest despite abnormal diastolic reserve. Echocardiography and other imaging can assess structure and some function, but they cannot confirm abnormal filling pressures during exercise on their own. Cardiac MRI at rest provides anatomy and function but not the dynamic, exercise-induced hemodynamic response. Hence, exercise PCWP measured invasively is the gold standard for establishing HFpEF.

For suspected cardiac sarcoidosis you want to know both where the heart has scar from prior inflammation and where there is currently active inflammation. Cardiac MRI with late gadolinium enhancement (LGE) is excellent at mapping scar and fibrosis, showing patchy, often basal or mid-wall LGE patterns and giving precise details about ventricular function. But MRI alone may miss areas of ongoing inflammation if there isn’t substantial scarring yet. FDG-PET CT adds metabolic insight by highlighting areas with active inflammatory activity, as those regions take up glucose highlighted by the tracer. With proper patient preparation to minimize normal myocardial glucose uptake, PET-CT can detect active disease that MRI might miss and can also reveal activity in other organs outside the heart, which helps confirm systemic sarcoidosis. Using both together combines their strengths: MRI defines structural involvement and functional impact, while PET-CT identifies active inflammation. This synergy increases diagnostic confidence, helps distinguish active disease from scar, and guides treatment decisions, such as whether to intensify immunosuppression and how to monitor response over time. That broader, more actionable information is why this imaging pair is considered the best approach for suspected cardiac sarcoidosis.

In hypertrophic obstructive cardiomyopathy, mechanical therapies are those that physically modify the outflow tract or septal anatomy. Dual-chamber pacing can alter the contraction sequence to reduce the LVOT gradient, alcohol septal ablation creates a controlled infarct to thin the septum, and open surgical myectomy surgically removes thickened septal tissue. Beta-blocker therapy is pharmacologic, aiming to reduce heart rate and contractility to lessen obstruction but it does not change the anatomy or physically relieve the obstruction. Therefore, beta-blocker therapy is not a mechanical treatment.

Coronary artery calcium scoring uses a CT scan to measure calcified plaque in the coronary arteries. In people with an intermediate 10-year ASCVD risk (around 5-20%), this test adds prognostic information beyond traditional risk factors and helps reclassify risk to guide preventive therapy. A zero CAC score can suggest lower short-term risk and may support a less aggressive approach if risk factors are favorable, while any detectable calcium indicates higher risk and can push toward initiating or intensifying statin therapy. Echocardiography, stress testing, and Holter monitoring assess heart structure, ischemia, or rhythm, not long-term ASCVD risk in asymptomatic individuals. Therefore, CAC scoring is the most appropriate tool to refine risk in this scenario.