Prognostic Implications of Coronary Artery Sclerosis in Troponin-Positive Patients with Non-Obstructive Coronary Arteries.

INTRODUCTION: Coronary sclerosis is a risk factor for the progression to obstructive coronary artery disease (CAD). However, understanding its impact on the outcomes of patients with myocardial infarction and non-obstructive coronary arteries is limited. This study aimed to explore the prognostic influence of coronary sclerosis on in- and out-of-hospital events in troponin-positive patients with non-obstructive coronary arteries. METHODS: This study was a retrospective cohort analysis based on prospectively collected data. A total of 24,775 patients who underwent coronary angiography from 2010 to 2021 in a German university hospital were screened, resulting in a final study cohort of 373 troponin-positive patients with non-obstructive coronary arteries and a follow-up period of 6.2 ± 3.1 years. Coronary sclerosis was defined as coronary plaques without angiographically detectable stenotic lesions of 50% or more in the large epicardial coronary arteries. The primary study endpoint was the occurrence of in-hospital events. Secondary endpoints included events during follow-up. RESULTS: Patients with coronary sclerosis were significantly older (70 ± 12 vs. 58 ± 16 years, p < 0.001), had ST-segment elevation less frequently on electrocardiogram (9.4% vs. 18.7%, p = 0.013), and suffered more often from diabetes mellitus (23.3% vs. 13.1%, p = 0.009), arterial hypertension (79.6% vs. 59.8%, p < 0.001), chronic obstructive pulmonary disease (17.1% vs. 9.4%, p = 0.028), chronic kidney disease (22.2% vs. 8.4%, p < 0.001), atrial fibrillation (19.8% vs. 12.2%, p = 0.045), and valvular diseases than patients without CAD. Patients with coronary sclerosis were more likely to receive medication for primary/secondary prevention on admission and at discharge. The incidence of in- and out-of-hospital events was significantly higher in patients with coronary sclerosis (in-hospital: 42.8% vs. 29.9%, p = 0.010; out-of-hospital: 46.0% vs. 26.1%, p < 0.001). Mortality rates tended to be higher in the coronary sclerosis group (29.4% vs. 20.0%, p = 0.066). CONCLUSION: Patients diagnosed with coronary sclerosis presented a higher incidence of comorbidities and increased medication use, and experienced higher rates of both in-hospital and out-of-hospital events, primarily due to the clustering of cardiovascular risk factors.

A Re-do Repair of Tetralogy of Fallot With an Anomalous Coronary Artery Using a Valved Conduit for the Right Ventricular Outflow Tract Reconstruction.

Several techniques can be used for the repair of right ventricular outflow tract (RVOT) stenosis in patients with an anomalous coronary artery. Here, we report a case of conduit obstruction after re-operation following double-tract reconstruction and release of stenosis by main pulmonary artery transection and conduit replacement. The patient is a female child diagnosed with tetralogy of Fallot with an anomalous coronary artery (right coronary across right ventricle outflow) who underwent correction with a double-tract RVOT repair at the age of 10 months (weight: 8 kg). At the age of eight years (weight: 24 kg), a conduit re-implantation procedure was required because of an increase in body weight. Designing smooth conduits proved challenging due to the anomalous coronary artery and a short main pulmonary arterial trunk. RVOT stenosis was documented early postoperatively, and further intervention was deemed necessary. At 13 years of age (weight: 45 kg), the patient underwent implantation of an adult-size valved conduit. Transection of the main pulmonary artery and extensive mobilization of the bilateral pulmonary arteries were effective in creating a relative laminar blood flow. Postoperative evaluations confirmed that the conduit was well-shaped and had satisfactory valve functionality. This case highlights the potential difficulties involved with replacing an additional conduit after double-tract cardiac repair procedures, particularly due to anatomical constraints posed by a coronary artery and a short pulmonary arterial trunk. Main pulmonary artery transection and comprehensive mobilization of branch pulmonary arteries can be a solution to conduit design difficulties in RVOT reconstruction after double-tract cardiac repair procedures.

Assessment of short-term results of thrombosuction during primary percutaneous coronary intervention in patients with acute myocardial infarction.

Aim: The study investigated the short-term outcomes of thrombosuction during primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction. Materials & methods: The study consisted of 57 patients who underwent primary or rescue PCI. The effect of thrombosuction on thrombolysis in myocardial infarction (TIMI) flow, failure to restore blood flow in the target vessel, and occurrence of mortality were reviewed in patients. Results: Thrombosis was performed in 45.61% of patients. Thrombosuction during PCI resulted in significant incremental TIMI-flow changes in this group of patients compared with patients who did just PCI. In 86.6%, these changes were three-degree and the initial TIMI-flow has changed from 0 to 3. Conclusion: The number of patients who underwent rescue PCI was higher than the smaller number of individuals who underwent thrombosuction.

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A Cardiologist's Clinical Dilemma: An Incidental Finding of a Potentially High-Risk Anomalous Right Coronary Artery Origin.

Coronary artery anomalies may place patients at risk for various adverse events. We present a case of a 62-year-old male with a two-year history of intermittent chest pain. A computed tomography coronary angiogram revealed a rare finding of an anomalous right coronary artery (ARCA) originating from the left ascending aorta, with high-risk features. This case highlights the complexities in diagnosing and managing ARCA, underscoring the importance of individualized care and careful consideration of invasive intervention risks versus potential benefits.

Intraindividual Comparison of Dose Reduction and Coronary Calcium Scoring Accuracy Using Kilovolt-independent and Tin Filtration CT Protocols.

Purpose To investigate the ability of kilovolt-independent (hereafter, kV-independent) and tin filter spectral shaping to accurately quantify the coronary artery calcium score (CACS) and radiation dose reductions compared with the standard 120-kV CT protocol. Materials and Methods This prospective, blinded reader study included 201 participants (mean age, 60 years ± 9.8 [SD]; 119 female, 82 male) who underwent standard 120-kV CT and additional kV-independent and tin filter research CT scans from October 2020 to July 2021. Scans were reconstructed using a Qr36f kernel for standard scans and an Sa36f kernel for research scans simulating artificial 120-kV images. CACS, risk categorization, and radiation doses were compared by analyzing data with analysis of variance, Kruskal-Wallis test, Mann-Whitney test, Bland-Altman analysis, Pearson correlations, and κ analysis for agreement. Results There was no evidence of differences in CACS across standard 120-kV, kV-independent, and tin filter scans, with median CACS values of 1 (IQR, 0-48), 0.6 (IQR, 0-58), and 0 (IQR, 0-51), respectively (P = .85). Compared with standard 120-kV scans, kV-independent and tin filter scans showed excellent correlation in CACS values (r = 0.993 and r = 0.999, respectively), with high agreement in CACS risk categorization (κ = 0.95 and κ = 0.93, respectively). Standard 120-kV scans had a mean radiation dose of 2.09 mSv ± 0.84, while kV-independent and tin filter scans reduced it to 1.21 mSv ± 0.85 and 0.26 mSv ± 0.11, cutting doses by 42% and 87%, respectively (P < .001). Conclusion The kV-independent and tin filter research CT acquisition techniques showed excellent agreement and high accuracy in CACS estimation compared with standard 120-kV scans, with large reductions in radiation dose. Keywords: CT, Cardiac, Coronary Arteries, Radiation Safety, Coronary Artery Calcium Score, Radiation Dose Reduction, Low-Dose CT Scan, Tin Filter, kV-Independent Supplemental material is available for this article. © RSNA, 2024.

Coronary artery thromboembolism as a cause of myocardial infarction with non-obstructive coronary arteries (MINOCA).

Acute myocardial infarction (AMI) usually represents the clinical manifestation of atherothrombotic coronary artery disease (CAD) resulting from atherosclerotic plaque rupture. However, there are cases in which coronary angiography or coronary computed tomography angiography reveals patients with acute coronary syndrome with non-obstructive CAD. This clinical entity is defined as myocardial infarction with non-obstructive coronary arteries (MINOCA) and often considered as a clinical dynamic working diagnosis that needs further investigations for the establishment of a final etiologic diagnosis. The main causes of a MINOCA working diagnosis include atherosclerotic, non-atherosclerotic (vessel-related and non-vessel-related), and thromboembolic causes This literature review aimed to investigate the major thromboembolic causes in patients presenting with MINOCA regarding their etiology and pathophysiologic mechanisms, as well as diagnostic and treatment methods.

Pulmonary, aorta, and coronary arteries post-arterial switch in transposition of great arteries: intermediate-term surveillance utilizing conventional echocardiography and cardiac multislice computed tomography.

BACKGROUND: Arterial switch operation (ASO) is the standard surgical choice for D-transposition of great arteries (D-TGA). However, the implications of ASO on pulmonaries, coronaries, and aorta have not been adequately investigated. The current study evaluates arterial morphologic changes post-ASO at intermediate-term surveillance. METHODS: From May 2021 to May 2022, patients with D-TGA who underwent ASO for more than six months were recruited. Preoperative and operative data were collected. Patients were assessed using echocardiography (ECHO) and multislice CT angiography (MSCT) to evaluate pulmonary, coronary, and aortic arterial anatomy. RESULTS: Twenty patients were included with median age of 11 (10-23.25) days at ASO and 14 (7.25-32.75) months on last follow-up. Neo-aortic regurgitation was detected in 12(60%) and neo-pulmonary regurgitation in 3 (15%). Using ECHO, complete evaluation of pulmonary arteries (PAs) was not achieved in 35% and incomplete coronaries assessment in 40% of cases. No stenosis was detected in coronaries using MSCT, although coronary anomalies were found in 9/20 (45%). Dilated Aortic annulus was detected in 16/20 (80%), dilated aortic root in 18/20 (90%), and dilated sinotubular junction in 70%. Right PA stenosis was diagnosed in 10/20 (50%) and left PA(LPA) stenosis in 7/20 (35%). Although Z-score of PAs did not correlate with aortic data, LPA bending angle was positively correlated to neo-aortic root diameter and Z-score (rho = 0.65,p = 0.016; rho = 0.69,p = 0.01), respectively. CONCLUSION: Echocardiography alone is not a conclusive surveillance tool for detecting late post-ASO anatomic changes in D-TGA patients. Cardiac MSCT should be considered for comprehensive evaluation on the intermediate-term follow-up post-ASO to accurately track morphologic abnormalities in the aorta, pulmonary, and coronary arteries.

Epicardium and Coronary Vessels.

Congenital anomalies and acquired diseases of the coronary blood vessels are of great clinical relevance. The early diagnosis of these conditions remains, however, challenging. In order to improve our knowledge of these ailments, progress has to be achieved in the research of the molecular and cellular mechanisms that control development of the coronary vascular bed. The aim of this chapter is to provide a succint account of the key elements of coronary blood vessel development, especially in the context of the role played by the epicardium and epicardial cellular derivatives. We will discuss the importance of the epicardium in coronary blood vessel morphogenesis, from the contribution of the epicardially derived mesenchyme to these blood vessels to its role as an instructive signaling center, attempting to relate these concepts to the origin of coronary disease.

Sex-specific differences in the mechanisms for enhanced thromboxane A2-mediated vasoconstriction in adult offspring exposed to prenatal hypoxia.

BACKGROUND: Prenatal hypoxia, a common pregnancy complication, leads to impaired cardiovascular outcomes in the adult offspring. It results in impaired vasodilation in coronary and mesenteric arteries of the adult offspring, due to reduced nitric oxide (NO). Thromboxane A2 (TxA2) is a potent vasoconstrictor increased in cardiovascular diseases, but its role in the impact of prenatal hypoxia is unknown. To prevent the risk of cardiovascular disease by prenatal hypoxia, we have tested a maternal treatment using a nanoparticle-encapsulated mitochondrial antioxidant (nMitoQ). We hypothesized that prenatal hypoxia enhances vascular TxA2 responses in the adult offspring, due to decreased NO modulation, and that this might be prevented by maternal nMitoQ treatment. METHODS: Pregnant Sprague-Dawley rats received a single intravenous injection (100 µL) of vehicle (saline) or nMitoQ (125 µmol/L) on gestational day (GD)15 and were exposed to normoxia (21% O2) or hypoxia (11% O2) from GD15 to GD21 (term = 22 days). Coronary and mesenteric arteries were isolated from the 4-month-old female and male offspring, and vasoconstriction responses to U46619 (TxA2 analog) were evaluated using wire myography. In mesenteric arteries, L-NAME (pan-NO synthase (NOS) inhibitor) was used to assess NO modulation. Mesenteric artery endothelial (e)NOS, and TxA2 receptor expression, superoxide, and 3-nitrotyrosine levels were assessed by immunofluorescence. RESULTS: Prenatal hypoxia resulted in increased U46619 responsiveness in coronary and mesenteric arteries of the female offspring, and to a lesser extent in the male offspring, which was prevented by nMitoQ. In females, there was a reduced impact of L-NAME in mesenteric arteries of the prenatal hypoxia saline-treated females, and reduced 3-nitrotyrosine levels. In males, L-NAME increased U46619 responses in mesenteric artery to a similar extent, but TxA2 receptor expression was increased by prenatal hypoxia. There were no changes in eNOS or superoxide levels. CONCLUSIONS: Prenatal hypoxia increased TxA2 vasoconstrictor capacity in the adult offspring in a sex-specific manner, via reduced NO modulation in females and increased TP expression in males. Maternal placental antioxidant treatment prevented the impact of prenatal hypoxia. These findings increase our understanding of how complicated pregnancies can lead to a sex difference in the programming of cardiovascular disease in the adult offspring.

Prenatal hypoxia, when the fetus does not receive enough oxygen, is a common problem during pregnancy that impacts the developing fetus. It is associated with an increased risk of cardiovascular disease in the offspring in adulthood. While the mechanisms are not fully understood, the blood vessel function in the offspring may be impacted by prenatal hypoxia. We hypothesize that prenatal hypoxia increases the constriction of the blood vessels in the offspring. The placenta, an essential organ for fetal development, supplies oxygen and nutrients to the fetus. In prenatal hypoxia pregnancies, the placenta does not work properly. We have been studying a placental treatment (called nMitoQ) to improve placenta function and thereby the blood vessel function of the offspring. We used a rat model of prenatal hypoxia, where pregnant rats (dams) were placed in a low oxygen environment (hypoxia) during the last trimester of pregnancy. Control rats were kept in normal oxygen conditions. The dams were treated with nMitoQ, or with saline (control). Next, we studied the blood vessels of the offspring in adulthood. We found that prenatal hypoxia increases the constriction of the blood vessels, which was prevented by treating the dams with nMitoQ. Interestingly, this impact was more severe in females compared to males, and the mechanisms were different between the sexes. This study helps in the understanding of how complicated pregnancies can impair cardiovascular health in the offspring, and in a potential development of targeted and sex-specific therapies for those offspring at high risk for future cardiovascular disease.

Beyond Coronary Artery Disease: Assessing the Microcirculation.

Ischemic heart disease (IHD) affects more than 20 million adults in the United States. Although classically attributed to atherosclerosis of the epicardial coronary arteries, nearly half of patients with stable angina and IHD who undergo invasive coronary angiography do not have obstructive epicardial coronary artery disease. Ischemia with nonobstructive coronary arteries is frequently caused by microvascular angina with underlying coronary microvascular dysfunction (CMD). Greater understanding the pathophysiology, diagnosis, and treatment of CMD holds promise to improve clinical outcomes of patients with ischemic heart disease.

The role of cardiac PET in diagnosis and prognosis of patients with ischemia with no obstructive coronary arteries (INOCA).

Chest pain, a common symptom in cardiovascular care, often leads to the investigation of obstructive coronary artery disease (CAD). However, many patients experience chest pain without obstructive CAD, termed INOCA (Ischemia with Non-Obstructive Coronary Arteries) or CMD (Coronary Microvascular Dysfunction). INOCA can be attributed to endothelial dysfunction, vascular smooth muscle dysfunction, or both, affecting about 20-30 % of patients with nonobstructive CAD. The diagnostic approach for INOCA includes both invasive and non-invasive methods, with cardiac PET (Positron Emission Tomography) playing a significant role in risk stratification and management. PET evaluates various parameters like myocardial blood flow under stress and rest, myocardial flow reserve, and myocardial ischemia. Such comprehensive assessment is essential in accurately diagnosing and managing INOCA, considering the complexity of this condition.

Effect of ivabradine on structural and functional changes of myocardium and NT-proBNP levels in patients with stable coronary heart disease after coronary stenting.

OBJECTIVE: Aim: To investigate the effect of ivabradine on the hemodynamics and contractility of the myocardium and the features of NT-pro-BNP production in patients with stable ischemic heart disease after endovascular revascularization of the myocardium depending on the number of affected coronary arteries during 12 months of therapy. PATIENTS AND METHODS: Materials and Methods: The object of the study was 120 patients with stable coronary artery disease: angina pectoris of functional class III with heart failure IIA FC III with preserved and moderately reduced ejection fraction of the left ventricle, who underwent coronary artery stenting. The examined patients were randomized according to the number of affected coronary vessels and the method of treatment. RESULTS: Results: Ivabradine in patients with stable ischemic heart disease after 12 months of therapy had a significant beneficial effect on the structural and functional parameters of the myocardium (contributed to the reverse remodeling of the left ventricle), which did not depend on the number of stented coronary arteries (p<0.05). In patients with stented one coronary artery, all structural and functional indicators of the heart after 12 months of treatment reached the values of practically healthy individuals from the control group. The use of ivabradine in patients with stable ischemic heart disease with heart failure with preserved and intermediate ejection fraction of the left ventricle after coronary stenting made it possible to ensure the correction of a number of clinical and pathogenetic links of the disease, which generally contributed to the improvement of metric and volumetric parameters of the heart. CONCLUSION: Conclusions: Ivabradine made it possible to significantly increase the effectiveness of standard therapy, which was manifested by a faster recovery of the geometry and contractility of the left ventricle. Therefore, the use of ivabradine along with standard therapy was appropriate for such a contingent of patients. The management of patients with stable coronary heart disease should combine adequate (surgical and pharmacological) treatment of the underlying disease, further individual medication correction of symptoms and circulatory disorders inherent in coronary heart disease and heart failure.

Coronary microvascular dysfunction and cancer therapy-related cardiovascular toxicity.

BACKGROUND: Coronary microvascular dysfunction (CMD) has been implicated as a potential mechanism in the pathophysiology of different clinical presentations, including ischemia and no obstructive coronary artery disease (INOCA), myocardial infarction and nonobstructive coronary arteries (MINOCA), stress cardiomyopathy, heart failure, and myocarditis. There are limited data about the role of CMD in cancer therapy-related cardiovascular toxicities. CASE PRESENTATIONS: Four women with a diagnosis of active cancer receiving treatment who developed subsequent MINOCA or INOCA presented for cardiac catheterization. Upon coronary angiography showing no obstructive coronary arteries, coronary function testing was performed to evaluate for CMD. METHODS: Coronary physiology was assessed measuring non-hyperemic (resting full-cycle ratio [RFR]) and hyperemic (fractional flow reserve [FFR]) indices using a physiologic pressure wire. The wire also measured coronary flow reserve (CFR), index of microcirculatory resistance (IMR), and RFR using thermodilution technology. CMD was confirmed if the CFR was <2.5 and the IMR was >25. RESULTS: Among 4 patients with diagnosis of active cancer presenting with chest pain, there was no evidence of obstructive coronary artery disease, leading to separate diagnoses of INOCA, MINOCA, stress cardiomyopathy, and myocarditis. We found CMD in 2 patients (1 with INOCA and 1 with immune checkpoint inhibitor-related myocarditis). CONCLUSIONS: CMD may play a role in cardiovascular toxicities. Further coronary physiology studies are needed to understand the mechanisms of cancer therapy-related cardiovascular toxicity and CMD, as well as optimal preventive and treatment options.

Comprehensive Two-Dimensional Pediatric Echocardiographic Nomograms for Coronary Artery Sizes in Caucasian Children and Comparison among Major Nomograms.

BACKGROUND: Although coronary artery nomograms in children have been published, data on Caucasian children are lacking. The aim of this study is to provide: (i) a full dataset of coronary artery diameters in healthy children and (ii) a comparison among major previous nomograms. MATERIALS AND METHODS: We prospectively evaluated 606 healthy subjects (age range, 1 days-<18 years; median age 8.7 years; 62.5% male). Coronary artery measurements in a short-axis view were performed. Age, heart rate, and body surface area (BSA) were used as independent variables in different analyses to predict the mean values of each measurement. To assess the accuracy of the predictive models of different studies, a Z-score calculator was created using Lopez's nomograms for comparison. RESULTS: The association with BSA was found to be stronger, and was used for normalization of our data. The best-fit models, satisfying the assumption of homoscedasticity and normality of residuals and showing the highest R2 scores, were logarithmic (ln[y] = a + b*ln[x]). Predicted values and Z-score boundaries by BSA are provided. Our ranges of normality are slightly lower than those, diverging from -0.22 to -0.59 Z-scores for the left main coronary artery and from -0.23 to -0.3 Z-scores for the right coronary artery. CONCLUSIONS: We report a complete dataset of normal echocardiography coronary artery diameter (including new measures of the proximal origin) values in a large population of healthy children. Our data were statistically like those of north American nomograms.

Immune-inflammatory biomarkers for the occurrence of MACE in patients with myocardial infarction with non-obstructive coronary arteries.

Background: Neutrophil-to-high-density lipoprotein cholesterol ratio (NHR), monocyte-to-high-density lipoprotein cholesterol ratio (MHR), lymphocyte-to-high-density lipoprotein cholesterol ratio (LHR), platelet-to-high-density lipoprotein cholesterol ratio (PHR), systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), and aggregate index of systemic inflammation (AISI) have been identified as immune-inflammatory biomarkers associated with the prognosis of cardiovascular diseases. However, the relationship of these biomarkers with the prognosis of myocardial infarction with non-obstructive coronary arteries (MINOCA) remains unclear. Method: Patients with MINOCA who underwent coronary angiography at the 920th Hospital of Joint Logistics Support Force were included in our study. Clinical baseline characteristics and laboratory testing data were collected from the hospital record system. The patients were divided into two groups on the basis of major adverse cardiovascular events (MACE) occurrence. Multiple logistic regression analysis was conducted to assess the relationship between NHR, MHR, LHR, PHR, SII, SIRI, AISI, and MACE. Receiver operating characteristic (ROC) curves were generated to evaluate the predictive value of NHR, MHR, LHR, PHR, SII, SIRI, and AISI for MACE in patients with MINOCA. The accuracy of the prediction was indicated by the area under the curve (AUC) value. Results: The study included 335 patients with MINOCA. (81 in the MACE group and 254 in the No-MACE group). The MACE group had higher levels of NHR, MHR, LHR, PHR, SII, SIRI, and AISI than the No-MACE group. Multiple logistic regression analysis adjusted for confounding factors indicated that the higher levels of NHR, MHR, PHR, SII, SIRI, and AISI were associated with the occurrence of MACE in patients with MINOCA (P < 0.001). The AUC values for NHR, MHR, PHR, SII, SIRI, and AISI were 0.695, 0.747, 0.674, 0.673, 0.688, and 0.676, respectively. The combination of NHR, MHR, PHR, SII, SIRI, and AISI improved the accuracy of predicting MACE in patients with MINOCA (AUC = 0.804). Conclusion: Higher levels of NHR, MHR, PHR, SII, SIRI, and AISI were associated with the occurrence of MACE, and the combination of NHR, MHR, PHR, SII, SIRI, and AISI improved the accuracy for predicting the incidence of MACE events in patients with MINOCA.

The Influence Of Epicardial Resistance On Microvascular Resistance Reserve.

BACKGROUND: The optimal index of microvascular function should be specific for the microvascular compartment. Yet, coronary flow reserve (CFR), despite being widely used to diagnose coronary microvascular dysfunction (CMD), is influenced by both epicardial and microvascular resistance. Conversely, microvascular resistance reserve (MRR) adjusts for fractional flow reserve (FFR), and thus is theoretically independent of epicardial resistance. OBJECTIVES: We tested the hypothesis that MRR, unlike CFR, is not influenced by increasing epicardial resistance, and thus is a more specific index of microvascular function. METHODS: In a cohort of 16 patients that had undergone proximal left anterior descending artery stenting, we created four grades of artificial stenosis (no stenosis, mild, moderate, and severe) using a coronary angioplasty balloon inflated to different degrees within the stent. For each stenosis grade, we calculated CFR and MRR using continuous thermodilution (64 measurements of each) in order to assess their response to changing epicardial resistance. RESULTS: Graded balloon inflation resulted in a significant sequential decrease in mean FFR (no stenosis: 0.82 ±0.05; mild: 0.72 ±0.04; moderate: 0.61 ±0.05; severe: 0.48 ±0.09, p<0.001). This translated into a linear decrease in mean hyperaemic coronary flow (no stenosis: 170.5 ±66.8 ml/min; mild: 149.8 ±58.8 ml/min; moderate: 124.4 ±53.0 ml/min; severe: 94.0 ±45.2 ml/min, p<0.001). CFR exhibited a marked linear decrease with increasing stenosis (no stenosis: 2.5 ±0.9; mild: 2.2 ±0.8; moderate: 1.8 ±0.7; severe: 1.4 ±0.6), corresponding to a decrease of 0.3 for a decrease in FFR of 0.1 (p<0.001). In contrast, MRR exhibited a negligible decrease across all stenosis grades (no stenosis: 3.0 ±1.0; mild: 3.0 ±1.0; moderate: 2.9 ±1.0; severe: 2.8 ±1.0), corresponding to a decrease of just 0.05 for a decrease in FFR of 0.1 (p<0.001). CONCLUSION: MRR, unlike CFR, is minimally influenced by epicardial resistance, and thus should be considered the more specific index of microvascular function. This suggests that MRR can also reliably evaluate microvascular function in patients with significant epicardial disease.

Casting Light on The Hidden Prevalence: A Novel Perspective on Hypoplastic Coronary Artery Disease.

Background and Objectives: Coronary artery anomalies (CAAs) represent a group of rare cardiac abnormalities with an incidence of up to 1.2%. The aim of this retrospective study was to conduct a comprehensive epidemiological assessment of the prevalence of hypoplastic coronary arteries using coronary computed tomography angiography (CCTA) in patients with diagnosed CAAs and individuals presenting with cardiovascular manifestations in the north-eastern region of Romania. This study was motivated by the limited investigation of the CAAs conducted in this area. Methods: We analyzed data collected from 12,758 coronary computed tomography angiography (CCTA) records available at the "Prof. Dr. George I.M. Georgescu" Cardiovascular Diseases Institute, spanning the years 2012 to 2022. Results: Among 350 individuals with CAAs (2.7% of the total cohort), 71 patients (20.3% of the anomaly presenting group and 0.5% of the entire CCTA cohort) exhibited at least one hypoplastic coronary artery. The mean age of individuals diagnosed with hypoplastic coronary artery disease (HCAD) was 61 years, while the age distribution among them ranged from 22 to 84 years. Nearly equal cases of right and left dominance (33 and 31, respectively) were observed, with only 7 cases of co-dominance. Conclusions: HCAD may be considered underexplored in current published research, despite its potentially significant implications ranging to an increased risk of sudden cardiac arrest. The specific prevalence of HCAD among CAAs might be higher than previously reported, possibly reflecting better diagnostic accuracy of CCTA over classic coronary imaging. The absence of standard diagnostic and therapeutic protocols for HCAD underscores the necessity of a personalized approach for such cases.

TAV-in-TAV in patients with prosthesis embolization: Impact of commissural alignment and global outcomes.

BACKGROUND: Optimal strategies to manage embolization of transcatheter aortic valve implantation (TAVI) devices are unclear; valve-in-valve (ViV) is often used. We aimed to describe through one-single center experience its rate, causes, consequences, and management as well as the rate and relevance of commissural alignment (CA) in this context. METHODS: We identified across 1038 TAVI cases, those cases requiring ViV for the management of first device embolization. CA (absence or mild misalignment) after first and second device was assessed by CT or fluoroscopy. RESULTS: A total of 23 cases (2.2%) were identified, 52.3% embolized towards the aorta and 47.7% towards the ventricle. Suboptimal implant height (38%) and embolization at the time of post-dilation (23%) were the most frequent mechanisms together with greater rate of bicuspid valve (p < 0.001) and a trend to greater annular eccentricity. Procedural and 1-year death occurred in 13% and 34%, respectively (vs. 1.1% and 7.8% in the global cohort, p < 0.001). CA was present in 76.9% of the prostheses initially implanted but was only spontaneously achieved in 30.8% of the second ViV device. Adequate CA of both prostheses was identified in only two cases (8.7%). There were no cases of coronary obstruction. CONCLUSIONS: TAVI device embolization mechanisms can often be predicted and prevented. Mortality following bail-out ViV is higher than in regular TAVI procedures but 2/3 of these patients survived beyond 1-year follow-up. In them, valve degeneration or coronary re-access might be particularly challenging since CA was rarely achieved with both devices suggesting that greater efforts should be made in this regard.

Cardiovascular pathology in vasculitis.

Vasculitides are diseases that can affect any vessel. When cardiac or aortic involvement is present, the prognosis can worsen significantly. Pathological assessment often plays a key role in reaching a definite diagnosis of cardiac or aortic vasculitis, particularly when the clinical evidence of a systemic inflammatory disease is missing. The following review will focus on the main histopathological findings of cardiac and aortic vasculitides.