Project description:Coronary cameral fistulas are abnormal communications between a coronary artery and a heart chamber or a great vessel which are reported in less than 0.1% of patients undergoing diagnostic coronary angiography. All three major coronary arteries are even less frequently involved in fistula formation as it is the case in our patient. A 68-year-old woman was admitted to cardiology clinic with complaints of exertional dyspnea and angina for two years and a new onset palpitation. Standard 12-lead electrocardiogram revealed atrial fibrillation (AF) with a ventricular rate of 114 beat/minute and accompanying T wave abnormalities and minimal ST-depression on lateral derivations. Transthoracic echocardiographic examination was normal except for diastolic dysfunction, minimally mitral regurgitation, and mild to moderate enlargement of the left atrium. Sinus rhythm was achieved by medical cardioversion with amiodarone infusion. Coronary angiography revealed diffuse and multiple coronary-left ventricle fistulas originating from the distal segments of both left and right coronary arterial systems without any stenosis in epicardial coronary arteries. The patient's symptoms resolved almost completely with medical therapy. High volume shunts via coronary artery to left ventricular microfistulas may lead to increased volume overload and subsequent increase in end-diastolic pressure of the left ventricle and may cause left atrial enlargement.
Project description:An 85-year-old man was admitted to the emergency department with chest pain. His electrocardiogram showed a right bundle branch block as well as increased voltages suggesting left ventricular hypertrophy and t-wave inversions consistent with a strain pattern (versus ischemia). He underwent echocardiography which showed regional noncompaction and associated hypokinesis. These findings led to coronary angiography which revealed multiple coronary-cameral fistulae involving all three coronary arteries. He was initially treated for acute coronary syndrome but after his diagnostic procedures this was narrowed to a beta blocker, to reduce myocardial oxygen demand, and an angiotensin-converting enzyme inhibitor due to the cardiomyopathy. Although the fistulae may have caused the patient's chest pain, intervention was not possible due to the diffuse nature of the fistulae. He did well in follow-up without the development of heart failure symptoms or continued angina. <Learning objective: Noncompaction cardiomyopathy and coronary cameral fistulae are two rare disorders that have even more rarely been described in a single patient. They may be a part of a spectrum of a single disease that results from arrest of the normal sequence of embryologic development of the heart. The management of the two conditions includes aspects of standard heart failure care as well as medical and possibly interventional therapy for coronary ischemia (angina) related to fistulae.>.
Project description:We describe about an elderly male presented to us with effort intolerance. He was diagnosed to have multiple coronary cameral fistulae and coronary pulmonary fistulae that gives an appearance of "Fountains In The Heart". Such a combined existence of biventricular coronary cameral fistulae and bilateral coronary artery to pulmonary artery fistulae is an unforeseen entity that has never been described before in an individual.
Project description:Wellens' syndrome refers to electrocardiographic (ECG) abnormalities in the precordial T-wave segment, which are associated with critical stenosis of the proximal left anterior descending (LAD) coronary artery. According to medical literature, this ECG abnormality is of paramount importance because this syndrome represents a preinfarction stage of coronary artery disease; however, same ECG pattern can also be seen in other conditions. Coronary fistula occurs due to anomalous communications between a coronary artery and a cardiac chamber or other vessel in the vicinity of the heart. We report a case of multiple coronary artery fistulae to the left ventricle in a 74-year-old woman who had a 2-year history of intermittent atypical chest pain and exercise dyspnea with positive criteria mimicking Wellens' syndrome without coronary atherosclerosis.
Project description:With improvements in survival from coronary artery disease (CAD) and an ageing population, refractory angina (RA) is becoming an increasingly common clinical problem facing clinicians in routine clinical practice. These patients experience chronic symptoms in the context of CAD, characterised by angina-type pain, which is uncontrolled despite optimal pharmacological, interventional and surgical therapy. Although mortality rates are no worse in this cohort, patients experience a significantly impaired quality of life with disproportionately high utilisation of healthcare services. It has been increasingly recognised that the needs of RA patients are multifactorial and best provided by specialist multi-disciplinary units. In this review, we consider the variety of therapies available to clinicians in the management of RA and discuss the promise of novel treatments.
Project description:BackgroundStudies that evaluate larger numbers of protein biomarkers in patients with coronary microvascular dysfunction (CMD) have not previously been performed, and very little is known concerning the pathogenetic mechanisms leading to CMD.Our objective was to analyze associations between a broad cardiovascular disease (CVD) protein biomarker assay and CMD, and further explore internal biomarker relations in order to identify possible targets for future treatment interventions.MethodsIn 174 women with angina pectoris and no significant obstructive coronary artery disease (<50% stenosis on invasive coronary angiography), CMD was assessed by transthoracic Doppler echocardiography measuring coronary flow velocity reserve (CFVR). Blood samples were analyzed with a CVD proteomic panel encompassing 92 biomarkers. The relation between biomarkers and CFVR was evaluated by regression analysis, and possible interrelations between significant biomarkers were investigated by principal component analysis (PCA).ResultsMedian age (SD) was 64?years (9.8), median CFVR (IQR) was 2.3 (1.9-2.7), and 28% of patients had CFVR?<?2.0. Eighteen biomarkers were significantly correlated with CFVR. In PCA, 8 of the biomarkers significantly related to CFVR showed high loadings on principal component 1 (PC1). The component scores of PC1 were significantly related to CFVR (p?=?0.002). The majority of the 8 interrelated PC1 biomarkers were related to the pro-inflammatory TNF-? - IL-6 - CRP pathway.ConclusionEighteen protein biomarkers were significantly associated with CMD. Eight biomarkers were interrelated in PCA, and share connection with pro-inflammatory pathways, highlighting a possible important role of inflammation in CMD.
Project description:BackgroundCirculating endothelial cells (CECs) are widely reported as a promising biomarker of endothelial damage/dysfunction in coronary artery disease (CAD). The two popular methods of CEC quantification include the use of immunomagnetic beads separation (IB) and flow cytometry analysis (FC); however, they suffer from two main shortcomings that affect their diagnostic and prognostic responses: non-specific bindings of magnetic beads to non-target cells and a high degree of variability in rare cell identification, respectively. We designed a microfluidic chip with spatially staggered micropillars for the efficient harvesting of CECs with intact cellular morphology in an attempt to revisit the diagnostic goal of CEC counts in CAD patients with angina pectoris.MethodsA label-free microfluidic assay that involved an in-situ enumeration and immunofluorescent identification (DAPI+/CD146+/VEGFR1+/CD45-) of CECs was carried out to assess the CEC count in human peripheral blood samples. A total of 55 CAD patients with angina pectoris [16 with chronic stable angina (CSA) and 39 with unstable angina (UA)], together with 15 heathy controls (HCs) were enrolled in the study.ResultsCEC counts are significantly higher in both CSA and UA groups compared to the HC group [respective medians of 6.9, 10.0 and 1.5 cells/ml (p < 0.01)]. Further, a significant elevation of CEC count was observed in the three UA subgroups [low risk (5.3) vs. intermediate risk (10.8) vs. high risk (18.0) cells/ml, p < 0.001) classified in accordance to the TIMI NSTEMI/UA risk score system. From the receiver-operating characteristic curve analysis, the AUCs for distinguishing CSA and UA from HC were 0.867 and 0.938, respectively. The corresponding sensitivities were 87.5% and 84.6% and the specificities were 66.7% and 86.7%, respectively.ConclusionsOur microfluidic assay system is efficient and stable for CEC capture and enumeration. The results showed that the CEC count has the potential to be a promising clinical biomarker for the assessment of endothelial damage/dysfunction in CAD patients with angina pectoris.