Clinical & Experimental Cardiology
Open Access

Physiological mechanism of Stress echocardiography

Amelia Hortan^{* *}Correspondence: Amelia Hortan, Department of Cardiology, Monash Victorian Heart Institute, Clayton, Australia, Email:

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Description

An established method for determining the degree and extent of coronary artery disease is stress echocardiography. Physical, pharmacological or electrical stress and echocardiography work together to diagnose myocardial ischemia with high accuracy. Inducible ischemia is characterized by a brief deterioration of regional function under stress. The diagnostic and prognosis accuracy of stress echocardiography is comparable to that of radioactive stress perfusion imaging or magnetic resonance, but it is far less expensive, has no negative effects on the environment, and poses no biohazards to the patient or the doctor. Its therapeutic impact has been supported by 35 years of research that is based on strong experimental, pathophysiological, technical, and clinical underpinnings.

Wall motion and coronary flow reserve, which are both measured in the left anterior descending artery, need to be combined into a single test. As technology and imaging quality advance, this strategy will become more and more practical. The potential for acquiring quantitative data that converts the existing qualitative assessment of regional wall motion into a number will be the next challenges in stress echo. The next hurdle for stress echocardiography is to get past its two biggest flaws: reliance on operator skill and a dearth of outcome data (a common issue in clinical imaging) that can be used to show how patient outcomes have improved. The primary indications for the clinical applications of stress echocardiography to ischemic heart disease are outlined in this study. 2D echocardiography combined with a physical, chemical, or electrical stress is known as stress echocardiography. The production of a momentary change in regional function under stress serves as the diagnostic endpoint for the diagnosis of myocardial ischaemia. Myocardial ischaemia is often caused by a temporary localized imbalance between oxygen demand and supply, and its symptoms can be utilised as a diagnostic tool. Myocardial ischaemia causes the traditional "cascade" of events, in which the different indicators are ranked one after the other in a clear timeline. Ischemia is preceded by flow heterogeneity, particularly between the subendocardial and subepicardial perfusion, metabolic alterations, changes in regional mechanical function, and only subsequently by pain and electrocardiographic abnormalities.

Chest pain is the least sensitive clinical sign of ischaemia, whereas regional malperfusion is the most sensitive, translating the pathophysiology idea of the ischemic cascade into practice.

The most frequent pathophysiological cause is a decrease in Coronary Flow Reserve (CFR). Ischaemia tends to spread centrifugally inside the ventricular cavity, regardless of the force applied or the morphological substrate; it first affects the subendocardial layer, only subsequently affecting the subepicardial layer if the ischaemia persists. Extravascular pressure is actually higher in the subendocardial layer than in the subepicardial layer, which results in a higher metabolic demand (wall tension is one of the key factors affecting myocardial oxygen consumption and a higher flow resistance).

CFR can be decreased in microvascular disease (such as syndrome X) or Left Ventricular (LV) hypertrophy even in the absence of Coronary Artery Disease (CAD) (e.g. arterial hypertension). When this syndrome exists, angina with Short Term (ST) segment depression and regional perfusion alterations might happen, usually without any abnormalities in the regional wall motion under stress. For the diagnosis of CAD, wall motion anomalies are more specific than CFR and/or perfusion alterations. Four equations that are centred on regional wall function and describe the four basic response patterns-normal, ischemia, necrotic, and viable-can be used to summarize all stress echocardiographic diagnoses. All significant cardiology guidelines suggest stress echocardiography in a variety of clinical scenarios.

Yet, due to its low cost, widespread availability, and absence of radiation exposure, its standing as a proven technology should encourage its clinical adoption as the preferred non-invasive imaging approach. Despite these distinctive characteristics, there is still an usage disparity with nuclear procedures perceived as more objective yet having equivalent diagnostic and prognosis accuracy. Exercise, inotropics and vasodilators can be used in a variety of ways to increase feasibility, avoid particular contraindications, and customize an evaluation for each patient.

Conclusion

As stress echocardiography reading shifts from a highly specialized qualitative method to a quantitative technique that would make it simpler for less specialized readers, a paradigm change will take place. Although technological bases are available, they have not yet developed to the point where they can be deployed on a regular basis in clinical settings. The majority of societal recommendations and recommendations are based on level C evidence and consensus. Large-scale prospective studies should be conducted to close the knowledge gap and support evidence-based treatment approaches.