Background: New onset of heart failure (HF) is an indication for the assessment of coronary artery disease. The aim of this study was to clarify the mechanistic causes of new onset HF associated with ischemic electrocardiograph (EKG) changes and chest pain in patients with patent or minimally diseased coronary arteries. Methods: Twenty consecutive patients (Group A) were retrospectively reviewed if they had an history of new onset of HF, chest pain, electrocardiographic changes indicating ischemia (ST depression or T wave inversion in at least two consecutive leads and a negative coronary angiogram [CA]) and did not require percutaneous coronary intervention or coronary artery bypass grafting. A 1:1 matched cohort (Group B) was adopted to validate the results. Results: All patients had a negative CA. The majority of subjects in Group A had a higher left ventricular end diastolic pressure (LVEDP) when compared to the control group (p<0.05). Similarly, the aortic diastolic (AOD) pressure was lower in Group A than in Group B (p<0.05). In patients with elevated LVEDP and low AOD, with a coronary perfusion pressure (CPP) <20 mmHg, deep T wave inversion in two consecutive leads were more frequently observed. When the CPP was between 20-30 mmHg, a mild ST depression were more frequently recorded (p30 mmHg, only mild non-specific ST-T changes or normal EKG were observed. Conclusions: In patients with HF and EKG changes suggestive of ischemia in at least two consecutive leads, a lower AOD could aggravate ischemia in patients with elevated left ventricular end diastolic pressure.

In the study of coronary artery disease (CAD), the mechanism of plaque formation and development is still an important subject for investigation. A limitation of current coronary angiography (CAG) is that it can only show static images of the narrowing of arterial channels without identifying the mechanism of the disease or predicting its progression or regression. To address this limitation, the CAG technique has been modified. The new approach emphasizes identifying and analyzing blood flow patterns, employing methodologies akin to those used by hydraulic engineers for fluid or gas movement through domestic or industrial pipes and pumps. With the new technique, various flow patterns and arterial phenomena—such as laminar, turbulent, antegrade, retrograde, and recirculating flow and potentially water hammer shock and vortex formation—are identified, recorded, and classified. These phenomena are then correlated with the presence of lesions at different locations within the coronary vasculature. The formation and growth of these lesions are explained from the perspective of fluid mechanics. As the pathophysiology of CAD and other cardiovascular conditions becomes clearer, new medical, surgical, and interventional treatments could be developed to reverse abnormal coronary flow dynamics and restore laminar flow, leading to improved clinical outcomes.

Background: In the study of coronary artery disease, the mechanisms underlying atherosclerosis initiation and progression or regression remain incompletely understood. Our research conceptualized the cardiovascular system as an integrated network of pumps and pipes, advocating for a paradigm shift from static imaging of coronary stenosis to dynamic assessments of coronary flow. Further review of fluid mechanics highlighted the water hammer phenomenon as a compelling analog for processes in coronary arteries. Methods: In this review, the analytical methodology employed a comprehensive, multifaceted approach that incorporated a review of fluid mechanics principles, in vitro acoustic experimentation, frame-by-frame visual angiographic assessments of in vivo coronary flow, and an artificial intelligence (AI) protocol designed to analyze the water hammer phenomenon within an acoustic framework. In the analysis of coronary flow, the angiograms were selected from patients with unstable angina if they had previously undergone one or more coronary angiograms, allowing for a longitudinal comparison of dynamic flow and phenomena. Results: The acoustic investigations pinpointed pockets of contrast concentrations, which might correspond to compression and rarefaction zones. Compression antinodes were correlated to severe stenosis, due to rapid shifts from low-pressure diastolic flow to high-pressure systolic surges, resulting in intimal injury. Rarefaction antinodes were correlated with milder lesions, due to de-escalating transitions from high systolic pressure to lower diastolic pressure. The areas of nodes remained without lesions. Based on the locations of antinodes and nodes, a coronary acoustic action map was constructed, enabling the identification of existing lesions, forecasting the progression of current lesions, and predicting the development of future lesions. Conclusions: The results suggested that intimal injury was likely induced by acoustic retrograde pressure waves from the water hammer phenomenon and developed new lesions at specifically exact locations.

Background: In the research of coronary artery disease, the precise initial injury that starts the atherosclerotic cascade remains unidentified. Moreover, the mechanisms governing the progression or regression of coronary plaque are not yet fully understood. Based on the concept that the cardiovascular system is a network of pumps and pipes, could fluid mechanics principles and practices elucidate the question of atherosclerosis using flow dynamics images from a novel angiographic technique, focusing on antegrade and retrograde flows and their collisions in iliac and coronary arteries? Methods: From January 2023 to May 2024, coronary angiograms of all hemodynamically stable patients with stable or unstable angina were screened. The angiograms displaying either no lesions (normal) or mild-to-moderate lesions were selected. Each patient underwent an evaluation of flow dynamics and arterial phenomena in both iliac and right coronary arteries. For each artery, data were categorized based on the following parameters: laminar versus non-laminar flow, presence versus absence of collisions, and presence versus absence of retrograde flow. Additionally, in two sub-studies, we analyzed the relationship between retrograde flow and blood pressure, and artificial intelligence algorithms were used to detect the retrograde flow in the right coronary artery. Results: A total of 95 patients were screened, and 51 were included in this study. The results comprised quantitative data (prevalence of laminar flows, collisions, and retrograde flows) and qualitative data (morphological characteristics of antegrade laminar flow, retrograde contrast flow, and instances of flow collision). The results showed that in the iliac artery, laminar flow was observed in 47.06% (24/51) of cases, with collisions noted in 23.53% (12/51). Retrograde flow was present in 47.06% (24/51) of cases, and notably, 75% (18/24) of these cases were associated with uncontrolled diastolic blood pressure (DBP) above 80 mmHg (p < 0.001). Conversely, in the RCA, laminar flow was observed in 54.9% (28/51) of cases, with collisions noted in only 3.92% (2/51). Retrograde flow was identified in 7.84% (4/51) of cases, and all these cases (100%, 4/4) were associated with uncontrolled systolic blood pressure (SBP) above 120 mmHg, though statistical significance was not reached due to the small sample size (p > 0.05). Conclusions: Based on the concept that the cardiovascular system is a network of pumps and pipes, this research methodology provides intriguing insights into arterial flow behaviors by integrating fluid mechanics practices with novel angiographic observations. The preliminary results of this study identified laminar flow as the predominant pattern, with retrograde flow and collisions occurring infrequently. The implications of vortex, collision, and disorganized flow highlight potential mechanisms for endothelial damage and atherosclerosis initiation. Moreover, the correlation with blood pressure underscores the critical role of hypertension management in preventing adverse hemodynamic events. Future directions include refining imaging techniques and further exploring the mechanistic links between flow dynamics and vascular pathophysiology to enhance diagnostic and therapeutic strategies for cardiovascular diseases.