European Journal of Cardiovascular Medicine

Cardiovascular disease remains a leading cause of illness and death worldwide. A critical aspect of this burden involves the interplay between coronary artery structure, systemic hemodynamic, particularly blood pressure, and myocardial remodelling, evidenced by alterations in left ventricular wall thickness [1]. Considering this interplay in the absence of significant epicardial coronary artery disease is an understudied but clinically important area, as it involves subclinical remodelling processes and potential initial markers of cardiovascular risk [2]

Coronary artery luminal diameter, typically assessed via coronary angiography, reflects not only anatomical size but the dynamic response of the vessel to systemic and local forces. Meanwhile, two-dimensional echocardiography facilitates non-invasive assessment of left ventricular wall thickness, enabling quantification of hypertrophy. Elevated systemic blood pressure, in both mean and diastolic components, serves as a potent driver of LV hypertrophy and arterial remodelling [3].

Studies have demonstrated that hypertensive individuals with left ventricular hypertrophy do not uniformly exhibit enlarged epicardial coronary arteries. One echocardiographic study comparing normotensive controls, athletes with physiological LVH, and hypertensive patients, both with and without LVH, found that the left main coronary artery lumen area was not increased in hypertensive LVH [4]. Interestingly, at higher systolic blood pressures, LMA area was inversely related to systolic pressure, despite being correlated with LV mass in the overall population. In difference, physiologic LVH was accompanied by increased LMA size, suggesting that pressure-independent stimuli might drive coronary remodelling differently than pressure overload does. [5]

A traditional understanding of coronary artery disease has long focused on the degree of luminal stenosis, as the principal determinant of myocardial ischemia and cardiovascular risk. This perspective, however, has evolved significantly with the advent of advanced intravascular imaging techniques and histopathological insights into atherogenesis. Increasing evidence reveals that the most dangerous coronary plaques are frequently not the ones causing serious luminal narrowing, but rather those that exhibit features of vulnerability, in spite of minimal obstruction. This phenomenon has profound implications for diagnosis, risk stratification, and management of coronary artery disease. [6]

Blood pressure control is essential not only for reducing afterload and LV hypertrophy but also for preventing plaque destabilisation. Taken together, existing evidence suggests a complex, multifactorial interplay among systemic blood pressure, left ventricular wall thickness, and coronary luminal geometry [7]. Elevated blood pressure is a powerful modifier of LV mass and is implicated in coronary atherosclerosis and vascular remodelling, even in subclinical stages. Until now, in hypertensive LVH, epicardial luminal enlargement is not guaranteed and may indeed be inversely related to systolic pressure, whereas physiologic LVH proves positive remodelling.

Understanding these gradations in patients without serious epicardial coronary artery disease is essential. This has both pathophysiological and clinical relevance: elucidating early remodelling may improve risk stratification, influence therapeutic methods, and enhance detection of vulnerable vascular segments [8]

The current study aims to fill this opening by investigating how coronary artery luminal diameter correlates with mean and diastolic blood pressure, and the degree of left ventricular wall thickening, on 2D echocardiography, in patients free of critical epicardial stenosis. By integrating hemodynamic variables with structural vascular and myocardial data, this study may advance our comprehension of early cardiovascular remodelling dynamics.

Research Design “ This prospective, observational, cross-sectional study was conducted in the Department of Cardiology at National Institute of Medical Science and Research, NIMS University, Jaipur, Rajasthan, a tertiary care centre equipped with high-resolution echocardiography systems and digital flat-panel cardiac catheterisation laboratories, over 18 months. The study included symptomatic patients suspected of having coronary artery disease who experienced both coronary angiography and transthoracic Doppler echocardiography. A overall of 100 consecutive patients were initially identified. Data collection involved demographic details such as age, gender, ethnicity, and body mass index, along with clinical information including the presence of hypertension, duration of hypertension, antihypertensive medication use, and the presence of left ventricular hypertrophy confirmed by imaging. Hemodynamic parameters, including mean arterial pressure, diastolic blood pressure, and resting heart rate, were recorded. Echocardiographic assessments were performed using a Philips Affiniti 50 2D Echocardiography machine under continuous ECG monitoring. Left ventricular interventricular septal thickness, posterior wall thickness, left ventricular ejection fraction, and LV mass index, obtained through standardised 2D echocardiography methods. Coronary angiographic assessment involved quantitative measurement of luminal diameters in the left main coronary artery, left anterior descending artery, left circumflex artery, and right coronary artery, focusing on reference segments unaffected by visible atherosclerotic narrowing. Digital images was analysed using quantitative coronary angiography software to measure luminal diameters of the major epicardial arteries in millimetres at proximal, mid, and distal reference segments free from angiographically significant stenosis. Following the acquisition of both imaging modalities, echocardiographic and angiographic datasets was matched for each patient, allowing for precise correlation of MAP, diastolic blood pressure, and LV wall thickness with coronary luminal diameters, thereby facilitating statistical assessment of their interrelationships. Other laboratory and clinical parameters were also recorded to provide a complete clinical profile of the study population. Inclusion Criteria  Adult patients aged 30–75 years.  Non-critical CAD, defined as <70% luminal stenosis in all major epicardial coronary arteries on coronary angiography.  Availability of complete echocardiographic assessment, including LV wall thickness Measurement, within one week of CAG.  Stable hemodynamic condition at the time of assessment. Exclusion Criteria  Critical CAD (>70% stenosis in any major epicardial artery).  Prior history of percutaneous coronary intervention or coronary artery bypass grafting.  Significant valvular heart disease (moderate to severe stenosis or regurgitation).  Left ventricular ejection fraction (LVEF) <50%.  Cardiomyopathy, congenital heart disease, or pericardial disease.  Poor echocardiographic imaging windows precluding accurate LV wall thickness measurement.  Acute coronary syndrome, decompensated heart failure, or arrhythmias at the time of evaluation.  Severe renal impairment (eGFR <30 mL/min/1.73 m²).  Refusal to participate or inability to provide informed consent Statistical analysis Statistical analysis was performed using SPSS software. Continuous variables were expressed as mean ± SD or median, and categorical variables as counts and percentages. Group comparisons used chi-square or Fisher’s exact test for categorical variables, and Student’s t-test, Mann-Whitney U test, one-way ANOVA, or Kruskal-Wallis test for continuous variables, as appropriate. Pearson’s correlation assessed variable relationships. Bivariate correlation was conducted between the blood pressure (systolic and diastolic) with that other parameters. A p-value < 0.05 was considered a significant difference.

The following results were observed in our study

Table 1 indicates that majority patients were elderly having the age mean of 63.35 ± 6.68 years and the BMI is in the average of 24.27 ± 1.39. Mean systolic blood pressure was 144.04 ± 10.03 mmHg and the mean value for the diastolic pressure was 79.85 ± 8.89 mmHg. Clinical parameters showed majority participants were smokers, accounting for 76%.

Table 2 shows that Haematological assessment have revealed the normal value for the haemoglobin which was 14.05 ± 0.57 g/dL, and the value of eGFR is 59.34 ± 5.6 ml/min/1.73 m², reveals slight abnormality associated with the renal function. Also the Inflammatory and cardiac biomarkers showed low level of hs-CRP 0.0504 ± 0.03 g/dL and the level of hs-Troponin T which is at 2.57 ± 0.99 pg/mL, indicating less systemic inflammation without any acute myocardial injury. Different lipid parameters demonstrated dyslipidemia with high amount of LDL which is 154 ± 23.84 mg/dL and the HDL is at 62.46 ± 7.51 mg/dL. However, the level of triglycerides is within the normal level of 127.36 ± 25.22 mg/dL.

Table 1: Different baseline parameters with their Mean ± SD values along with the frequency and percentage of smoker and non-smoker.

Table 2: The blood parameters and the TTDE parameters with their Mean±SD values.

Table 3 Shows Echocardiographic parameters revealed mean LVEF of 51.71±15.04, with LVED  56.12 ± 8.75 mm and LVESD  36.09 ± 8.09 mm. The thickness of the wall is normal at IVSWT: 10.43 ± 2.95 mm; LVPWT: 10.76 ± 2.95 mm. The deceleration time for the diastolic parameters is 148.26 ± 40.93 msec. The dimension at the left atrium is 39.84 ± 6.67 mm. TRPG is 29.42 ± 10.17 mmHg is within the normal limits, thus there is no associated pulmonary hypertension.

Table 4 Demonstartes different invasive coronary angiography findings. The stenosis morphology evaluation has revealed 51% of concentric and 49% of eccentric lesions and 47% of aneurysm or dissection was observed. Left circumflex artery lesion was seen in 30%, left anterior descending artery lesion in 26%, right coronary artery 24% and left main coronary artery 20%.  The mean of severity of lesion was 59.76 ± 4.28% and the average length of the lesion was 12.75 ± 4.48 mm. The evaluation of the functional assessment reveals the impaired coronary physiology, having the mean values for the coronary flow as CFR: 2.14 ± 0.28 and the FFR is 0.88 ± 0.06.

Table 3: The  TTDE parameters with their Mean±SD values

Table 4: The data findings related to the coronary angiography

Table 5 Evaluates the correlation between the parameters related to the blood pressure and the involvement of the coronary artery. Systolic and diastolic blood pressures showed positive correlation of values r = 0.242, p = 0.015, which indicates the high level of diastolic blood pressure. It also shows Negative correlation of systolic blood pressure with coronary arteries. Values are

r = –0.627, p < 0.01 with LMCA, r = –0.684, p < 0.01 with left anterior descending, r = –0.602, p < 0.01 with left circumflex, r = –0.667, p < 0.01 with right coronary artery. Also negative correlations is observed in case of diastolic pressure, the value of LM is r = –0.331, p = 0.001, the value of LAD is r = –0.329, p = 0.001 and LCX is r = –0.377, p < 0.01, RCA is r = –0.298, p = 0.003, which shows weak strength in comparing to the systolic pressure. 

Table 5: The values for the bivariate correlation between the blood pressure and the diameter of the coronary artery

Table 6, the bivariate correlation between blood pressure, transthoracic Doppler echocardiography (TTDE) parameters, and invasive coronary angiography (ICA) reveals several significant findings. Systolic blood pressure (SBP) shows a significant positive correlation with lesion severity (r = 0.242, p = 0.015), indicating that higher systolic pressure is associated with more severe coronary artery lesions. SBP also negatively correlates with the LV mass index (r = -0.231, p = 0.02), which implies that higher systolic blood pressure might lead to increased left ventricular mass. Additionally, SBP is significantly negatively correlated with the E/A ratio (r = -0.227, p = 0.023), an indicator of diastolic function. Diastolic blood pressure (DBP) shows a significant negative correlation with LVEDD (r = -0.321, p < 0.001), indicating that higher DBP may be associated with smaller left ventricular chamber size, possibly reflecting a compensatory response to chronic pressure overload.

Table 6: Bivariate Correlation between blood pressure, TTDE, and Invasive Coronary Angiography parameters

A study assessed the correlation between coronary artery disease (CAD) and left ventricular hypertrophy (LVH) and CCA-IMT as measured by the Radio Frequency-Quality Intima-Media Thickness. RFQIMT is an advanced technique of ultrasound assessment of the carotid. Its accuracy in general would assist in the count of the coronary lesions in patients with at least one significant major epicardial coronary vessel stenosis [09].

An evaluation with an ECG-gated 320-detector- row CT scanner was done on the association between LV mass and geometry and coronary artery disease. The independent predictor of higher CAD-RADS, after controlling septal wall thickness, is the LV geometric pattern. Concentric hypertrophy is the most significant predictor of high CAD-RADS amongst abnormal geometric patterns of LV [10].

A study evaluated the epicardial coronary arteries luminal diameter among patients with PAH.  A retrospective study of PAH that included fifty patients who underwent cardiac computed tomography (CT) angiography at the centre. PAH could be related to the enlargement of the right coronary artery diameter [11].

A study examined the association between the left ventricular end-diastolic pressure (LVEDP) assessed by left cardiac catheterisation and coronary artery disease and its severity and degree, that of coronary angiography (CAG). Summarily, the results indicate that there was a high level of association between elevated LVEDP and CAD and the extent and severity of the same. Only non-CAD patients showed a correlation of LVEDP with age. Measurement of LVEDP generates add-on clinical value in CAD and non-CAD patients [12].

Dodge et al. studied the influence of LV hypertrophy or dilation on Coronary Artery lumen Diameter. The authors have proposed that the enlargement of the coronary artery lumen could be an adaptive process that arises to satisfy the incrementally increased flow requirement of the myocardium [13].

In a study conducted by Lin et al., [14] showed severity of obstructive and non-obstructive CAD that were linked with increased LVEDP. The earlier research indicated that the decrease in left ventricular compliance was in extraordinary agreement with the level of severity of CAD [15]. Paul et al. [16] concluded that severity of the ischemia decides the incidence and the extent of the Diastolic Dysfunction. Abnormal diastolic functioning can, on the other hand, also indicate the level of ischemia. Perrone-Filardi et al., [17] demonstrated that in CAD patients, the worse the left ventricular filling and regional asynchrony, the higher the degree of ischemia, indicating a higher extent of jeopardized myocardium, occurred in patients without evidence of significant impairment in left ventricular systolic function during rest. In another study, it was also noted that patients with poor LV relaxation showed worse CAD [18]. Nevertheless, as it was demonstrated by Abalı G et al. [19], the diastolic function failed to depict any kind of impairment in the patients regarding the severity of the CAD. However, in the study of Abali et al., the predictive value of E/Em to have high left ventricular diastolic pressures was poor because the diastolic function was tested by echocardiography. Mitral flow is related to various interconnected factors; thus, it has not been possible to find out the diastolic function of the patient using the velocity curves of the mitral flow of many of the populations of patients [20].

This study demonstrates that systolic and diastolic blood pressure significantly influence coronary luminal diameters, while LV wall thickness positively associates with epicardial artery size. These relationships, observed in patients without critical stenosis, underscore the interplay between systemic hemodynamic stress and myocardial adaptation. The findings support stringent blood pressure management as a strategy to preserve coronary structure and function and suggest that early detection of vascular remodeling may aid in risk stratification and preventive care in non-obstructive coronary disease.

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