Coronary Artery Narrowing Research Articles

INCENTIVE SPIROMETRY AND DEEP BREATHING EXERCISE PREFER TO PREVENT DECREASED OF LUNG VITAL CAPASITY AS GOOD AS DEEP BREATHING EXERCISE POST CORONARY ARTERY BYPASS GRAFT PHASE I

Coronary artery bypass graft (CABG) is a procedure to remove the blood vessels from internal mammary artery, radial artery or vein saphenus and to the surface of the heart to create a bypass in coronary artery narrowing. Data taken from the patients with heart disease from medical department of rehabilitation H.Adam Malik Medan who undergoing coronary bypass graft surgery. From 73 patients with post-cardiac surgery who were referred to the Medical Rehabilitation, 49 people were post-CABG (in 2010), and 57 people in 2011. General anesthesia, diaphragmatic dysfunction, abdominal distension, changes in chest wall, surgical wound, pleural effusion, pain and dysfunction of the respiratory muscles, may lead to reduction in lung vital capasity of up to 55% post operative. Intervention were incentive spirometry and breathing exercise. The purposes of this study is knowing whether the intervention incentive spirometry and breathing exercise can more minimize the decline in lung capasity than breathing exercise intervention only on post-CABG in phase I. Experimental research with non-probability sampling two group pre test and post test design . Subjects of group I (n = 9) receive incentive spirometry (IS) and deep breathing exercises (DBE), while group II (n=9) receive only a deep breathing exercise. Data analysis with paired samples t-test suggested the mean value of vital capasity (VC) from group I (IS and DBE) was 73.78% (pre op) after 6 days postoperatively decreased to 59.56, average decline in 14.22, P = 0.002. While the VC on group II (DBE) was 74.11 after 6 days postoperatively decreased to 55.78. Average reduction was 18, 33, p value = 0.0001. There was no significantly differences between group I and group II from statistical analysis Independent t-test, with p-value = 0.512 (p>0.05). Conclusions of this study: There was a significant effect of incentives spirometry and deep breathing exercises in preventing the decrease of lung vital capasity in post-CABG patients, There was a significant influence provision of deep breathing exercises in preventing the decrease of lung vital capasity, There were no significant differences between treatment combinations of incentive spirometry and deep breathing exercises with deep breathing exercises only in preventing the decrease of lung vital capasity in post-CABG, with a p-value = 0.512

CRYPTIC CHEST PAIN: WELLEN’S SYNDROME DUE TO MYOCARDIAL BRIDGING

SESSION TITLE: Cardiovascular Disease 2 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Chest pain of cardiac origin is commonly ischemic in etiology. However, the phenomenon of myocardial bridging as a cause of chest pain has come to attention recently. Herein, an epicardial coronary artery develops a transient myocardial course. During systole, a portion of the vessel is mechanically compressed and results in ischemia. This has been attributed to as a rare cause of angina. Here we present our experience with a patient who was diagnosed with the same. CASE PRESENTATION: A 51 year old man with no past medical history, presented to the emergency room with pressure like chest pain of two days duration. He had multiple episodes of pain and each lasted for around 20 minutes. It was associated with palpitations, and exacerbated by physical exertion. He was a former smoker and reportedly quit smoking 20 years back. His blood pressure was 153/95 mmHg; temperature 98.1F; heart rate 73/min regular; respiratory rate 18/min. ECG showed Type 1 Wellen's biphasic pattern in V2, V3. Three sets of cardiac troponins were normal. Wellens pattern on ECG is highly specific (89%) for critical left anterior descending artery (LAD) stenosis. [1] [2]. Therefore, the patient was sent for emergent cardiac catheterization. Coronary angiography revealed normal left main, left circumflex and right coronary artery. However, LAD artery showed moderate myocardial bridging. DISCUSSION: In myocardial bridging, a coronary artery that normally runs on the epicardium, develops a transient intra-myocardial course. This section of the artery gets compressed during ventricular systole. Generally asymptomatic, bridging sometimes results in angina, arrhythmias myocardial ischemia. Most myocardial bridging has been found to occur in the middle portion of the LAD artery. However, on autopsy right coronary and left circumflex arteries have shown bridging at comparable rates. [3]. Proximal portion of the bridged segment is prone to accelerated atherosclerosis.Hypertrophic obstructive cardiomyopathy (HOCM) has shown increased association with myocardial bridging. Treatment is with beta blockers and non-dihydropyridine calcium channel blockers. Therapeutic benefit results from decreased chronotropy and inotropy. In cases refractory to medical management, surgical myotomy, coronary artery stenting or coronary artery bypass grafting (CABG) can be pursued. Our patient was started on aspirin, amlodipine, metoprolol, and rosuvastatin. His hospital course was uneventful and he was discharged on pharmacological therapy. CONCLUSIONS: Myocardial Bridging is being recognized increasingly as a cause of refractory angina. However, it is still not widely included as a differential diagnosis. Since the treatment is fairly specific, we wish to underscore the importance of recognizing myocardial bridging as an atypical cause of chest pain. Reference #1: C. de Zwaan, F.W. Bar, H.J. Wellens. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J, 103 (1982), pp. 730-736. Reference #2: C. de Zwaan, F.W. Bar, J.H. Janssen, et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. . Am Heart J, 117 (1989), pp. 657-665. Reference #3: Polacek P, Kralove H. Relation of myocardial bridges and loops on the coronary arteries to coronary occlusions. Am Heart J. 1961;61:44-52 DISCLOSURES: No relevant relationships by Paurush Ambesh, source=Web Response No relevant relationships by Stephan Kamholz, source=Web Response No relevant relationships by Dikshya Sharma, source=Web Response No relevant relationships by Ankur Sinha, source=Web Response

CORRELATION BETWEEN PLATELET TO LYMPHOCYTE RATIO AND CORONARY ARTERY NARROWING

Coronary Heart Disease (CHD) is one of the most common diseases of the cardiovascular system, characterized by atherosclerotic lesions. Atherosclerotic vascular processes are multifactorial. One of the factors is the process of inflammation. Platelet to Lymphocyte Ratio (PLR) is a marker that predicts the atherosclerotic coronary burden. The purpose of this research was to determine the correlation between platelet to lymphocyte ratio and coronary artery narrowing in CHD patients. This research was an analytical observation with a cross-sectional design, conducted on 54 patients with CHD who underwent angiography at the Adam Malik Hospital, Medan in February–October 2016. We examined platelet count, absolute lymphocyte count and percentage of coronary artery narrowing and coronary artery narrowing in CHD patients. There is a weak correlation between platelet to lymphocyte ratio and coronary artery narrowing in CHD patients ((r=0.276)). The result of the statistic test showed no significant correlation of platelet to lymphocyte ratio and coronary artery narrowing patients (p=0.043). In this study there is a weak correlation between platelet to lymphocyte ratio and coronary artery narrowing in CHD patients.

Chronic Stable Angina

By definition, chronic stable angina is angina that has been stable with regard to frequency and severity for at least 2 months. Chronic stable angina is the initial manifestation of coronary heart disease in approximately 50% of patients. Typically, this type of angina occurs in the setting of atherosclerotic coronary arterial narrowing, although other causes are possible. This review covers the epidemiology, pathophysiology, initial evaluation, differential diagnosis, management, and treatment of patients with chronic stable angina. Figures show noninvasive testing and the probability of coronary artery disease; diagnosis of patients with suspected ischemic heart disease; probability of severe coronary artery disease; coronary outcomes for high- versus low-intensity statin therapy; optimal medical therapy (OMT) versus OMT and percutaneous coronary intervention for chronic angina; OMT versus percutaneous coronary intervention for stable coronary heart disease; and coronary artery bypass grafting versus percutaneous coronary intervention for diabetes and coronary artery disease. Tables list the grading of angina pectoris by the Canadian Cardiovascular Society classification system, the differential diagnosis of chest pain, conditions promoting myocardial oxygen supply and demand mismatch, the features of typical angina, the classification of chest pain, a comparison of the pretest likelihood of coronary heart disease (CHD) in low-risk and high-risk symptomatic patients, the posttest probability of significant CHD based on pretest probabilities of CHD and normal or abnormal results of noninvasive studies, survival according to risk groups based on Duke treadmill scores, high- and moderate-intensity statin therapy, revascularization to improve survival compared with medical therapy, revascularization to improve symptoms with significant anatomic (≥ 50% left main or ≥ 70% nonleft main coronary artery disease) or physiologic (fractional flow reserve ≤ 0.80) coronary artery stenoses, and questions recommended by an expert panel for patients with chronic stable angina at follow-up visits. This review contains 7 highly rendered figures, 13 tables, and 109 references.

Chronic Stable Angina

By definition, chronic stable angina is angina that has been stable with regard to frequency and severity for at least 2 months. Chronic stable angina is the initial manifestation of coronary heart disease in approximately 50% of patients. Typically, this type of angina occurs in the setting of atherosclerotic coronary arterial narrowing, although other causes are possible. This review covers the epidemiology, pathophysiology, initial evaluation, differential diagnosis, management, and treatment of patients with chronic stable angina. Figures show noninvasive testing and the probability of coronary artery disease; diagnosis of patients with suspected ischemic heart disease; probability of severe coronary artery disease; coronary outcomes for high- versus low-intensity statin therapy; optimal medical therapy (OMT) versus OMT and percutaneous coronary intervention for chronic angina; OMT versus percutaneous coronary intervention for stable coronary heart disease; and coronary artery bypass grafting versus percutaneous coronary intervention for diabetes and coronary artery disease. Tables list the grading of angina pectoris by the Canadian Cardiovascular Society classification system, the differential diagnosis of chest pain, conditions promoting myocardial oxygen supply and demand mismatch, the features of typical angina, the classification of chest pain, a comparison of the pretest likelihood of coronary heart disease (CHD) in low-risk and high-risk symptomatic patients, the posttest probability of significant CHD based on pretest probabilities of CHD and normal or abnormal results of noninvasive studies, survival according to risk groups based on Duke treadmill scores, high- and moderate-intensity statin therapy, revascularization to improve survival compared with medical therapy, revascularization to improve symptoms with significant anatomic (≥ 50% left main or ≥ 70% nonleft main coronary artery disease) or physiologic (fractional flow reserve ≤ 0.80) coronary artery stenoses, and questions recommended by an expert panel for patients with chronic stable angina at follow-up visits. This review contains 7 highly rendered figures, 13 tables, and 109 references.

Characteristics of sauna deaths in Korea in relation to different blood alcohol concentrations

Although the benefits of sauna bathing have been demonstrated in epidemiological studies, sauna deaths have been reported. The aim of this study was to determine the demographic and forensic characteristics associated with different blood alcohol concentrations (BACs) in sauna deaths in Korea. In this retrospective analysis, data were collected from a nationwide pool in Korea between January 2008 and December 2015 to determine the role of alcohol intoxication in sauna deaths based on the subjects’ BAC and to evaluate the demographic and forensic characteristics associated with different BACs. One hundred and three deaths were classified into 2 groups: the non-intoxication (NI) group (BAC,<0.08%; n = 27) and the intoxication (I) group (BAC,≥0.08%; n = 76). Demographic and forensic characteristics were compared between the groups using a multinomial logistic regression analysis. The proportions of decedents who were male (odds ratio: 17.4, 95.0% confidence interval: 3.8–79.8) and in a prone position at the scene of death (odds ratio: 11.3, 95.0% confidence interval: 2.1–60.1) were significantly higher (P < 0.001 and P < 0.05, retrospectively) in the I group than in the NI group. However, no significant differences were observed with respect to obesity, coronary artery narrowing, and liver pathology. Sauna deaths exhibited different characteristics according to BACs detected at autopsy. The differences in sauna deaths between the I and NI groups may have implications for the targeted prevention of sauna deaths associated with alcohol consumption.

Role of Fibroblast Growth Factor- 23 in Coronary Artery Diseases and its Association with Apolipoprotein A1

Coronary artery disease (CAD) is a clinical manifestation resulting from a narrowing of epicardial coronary arteries that supply blood and oxygen to the heart. Coronary artery disease is mostcommonlydue to atherosclerotic occlusion of the coronary arteries.Fibroblast growth factor 23 (FGF23) is a circulating peptide hormone secreted by bone cells,regulating phosphate and vitamin D metabolism. Several recent observational studies reported an independent association of circulating FGF23 with several cardiovascular disease (CVD) risk factors including left ventricular hypertrophy and vascular dysfunction,CVD progression and incident clinical CVD eventsand mortality.Apolipoprotein A1 (ApoA1) is the primary protein associated with high-density lipoprotein (HDL) particles,and plays a central role in reverse cholesterol transport. HDL cholesterol (HDL-C) and ApoA1 concentrations are inverlassely related to the risk for coronary artery disease. To find the role of fibroblast growth factor-23 in coronary artery disease and its associationwith Apolipoprotein-A1.This ccross –sectionalstudyincluded 42 elective patients attending the cardiology unit and the results of those patients were compared with 40 healthy control group. Blood samples were obtained for measurements of (FGF-23,troponin I,Apo-A1,total creatine kinase activity,urea,creatinine and lipid profile).The obtained results showed that there was a significant difference in serum FGF-23 in coronary artery disease (367.52 ± 128.52 pg/ml) as compared with the control (165.41 ± 53.65 pg/ml) (p&lt; 0.05). There was a significant differences in Apo-A1 in coronary artery disease (2.03±0.90 mg/ml) as compared with the control (1.49 ± 0.25 mg/ml) (P = 0.014).There was a significant difference in age between CAD (58.66±8.85) and control group (51.125 ± 11.71) (P&lt;0.005).There was a significant difference in TG where control (99.50 ± 21.59) differ from CAD (142.05 ± 66.24) (P = 0.006).According to the results that were shown in the tables, we can be conclude that higher levels of FGF23 and Apo-A1 may be associated with complications and mortality of CAD beside its associating with atherosclerosis in the Iraqi patients.

Deep Learning for Prediction of Obstructive Disease From Fast Myocardial Perfusion SPECT: A Multicenter Study

ObjectivesThe study evaluated the automatic prediction of obstructive disease from myocardial perfusion imaging (MPI) by deep learning as compared with total perfusion deficit (TPD). BackgroundDeep convolutional neural networks trained with a large multicenter population may provide improved prediction of per-patient and per-vessel coronary artery disease from single-photon emission computed tomography MPI. MethodsA total of 1,638 patients (67% men) without known coronary artery disease, undergoing stress 99mTc-sestamibi or tetrofosmin MPI with new generation solid-state scanners in 9 different sites, with invasive coronary angiography performed within 6 months of MPI, were studied. Obstructive disease was defined as ≥70% narrowing of coronary arteries (≥50% for left main artery). Left ventricular myocardium was segmented using clinical nuclear cardiology software and verified by an expert reader. Stress TPD was computed using sex- and camera-specific normal limits. Deep learning was trained using raw and quantitative polar maps and evaluated for prediction of obstructive stenosis in a stratified 10-fold cross-validation procedure. ResultsA total of 1,018 (62%) patients and 1,797 of 4,914 (37%) arteries had obstructive disease. Area under the receiver-operating characteristic curve for disease prediction by deep learning was higher than for TPD (per patient: 0.80 vs. 0.78; per vessel: 0.76 vs. 0.73: p < 0.01). With deep learning threshold set to the same specificity as TPD, per-patient sensitivity improved from 79.8% (TPD) to 82.3% (deep learning) (p < 0.05), and per-vessel sensitivity improved from 64.4% (TPD) to 69.8% (deep learning) (p < 0.01). ConclusionsDeep learning has the potential to improve automatic interpretation of MPI as compared with current clinical methods.

Tropical Coronary Artery Disease and Arrhythmogenic Potentials—The Changing Pattern towards Endomyocardial Fibrosis—An Analysis

Aim: To analyse the increasing burden of coronary artery disease (CAD) in tropical and subtropical belts of the Equator since it remains blurred and carries a grim prognosis. Introduction: Endomyocardial fibrosis [EMF] is a tropical febrile disorder, confined to peculiar and limited geographical areas. Plaque buildup in endocardium and coronary arteries, causing ischemic injury and arrhythmic episodes, is a vanishing mystery in its pathogenesis and emphasizing alternative routes for understanding and treatment of this enigmatic disease. Case Report: 15 cases in various age groups were reported with potential complications of coronary artery disease and arrhythmias, associated with endocardial lesions, the characteristic feature of endomyocardial fibrosis. Conclusion: The narrowing of coronary arteries as a result of thickening of the walls, spasm, inflammation, plaques and its rupture produce ischemic episodes which can occur slowly or suddenly in a devastating pattern with arrhythmogenic potentials. The important steps to prevent and decrease the risk of CAD is to reduce the chance of getting this disorder by epidemiological measures with an advice of blood thinning medications such as small daily dose aspirin, antibiotics in susceptible individuals and revascularization in established myocardial infarction.

Assessment of atherosclerotic luminal narrowing of coronary arteries based on morphometrically generated visual guides.

Determination of the degree of stenosis of atherosclerotic coronary arteries is an important part of postmortem examination of the heart, but, unfortunately, estimation of the degree of luminal narrowing can be imprecise and tends to be approximations. Visual guides can be useful to assess this, but earlier attempts to develop such guides did not employ digital technology. Using this approach, we have developed two computer-generated morphometric guides to estimate the degree of luminal narrowing of atherosclerotic coronary arteries. The first is based on symmetric or eccentric circular or crescentic narrowing of the vessel lumen and the second on either slit-like or irregularly shaped narrowing of the vessel lumens. Using the Aperio ScanScope XT at a magnification of 20× we created digital whole-slide images of 20 representative microscopic cross sections of the left anterior descending (LAD) coronary artery, stained with either hematoxylin and eosin (H&E) or Movat's pentachrome stain. These cross sections illustrated a variety of luminal profiles and degrees of stenosis. Three representative types of images were selected and a visual guide was constructed with Adobe Photoshop CS5. Using the "Scale" and "Measurement" tools, we created a series of representations of stenosis with luminal cross sections depicting 20%, 40%, 60%, 70%, 80%, and 90% occlusion of the LAD branch. Four pathologists independently reviewed and scored the degree of atherosclerotic luminal narrowing based on our visual guides. In addition, digital technology was employed to determine the degree of narrowing by measuring the cross-sectional area of the 20 microscopic sections of the vessels, first assuming no narrowing and then comparing this to the percent of narrowing determined by precise measurement. Two of the observers were very experienced general autopsy pathologists, one was a first-year pathology resident on his first rotation on the autopsy service, and the fourth observer was a highly experienced cardiovascular pathologist. Interobserver reliability was assessed by determination of the intraclass correlation coefficient. The degrees of agreement for two H&E- and Movat-stained sections of the LADs from each of 10 decedents were 0.874 and 0.899, respectively, indicating strong interobserver agreement. On the average, the mean visual scores were ~8% less than the morphometric assessment (52.7 vs. 60.2), respectively. The visual guides that we have generated for scoring atherosclerotic luminal narrowing of coronary arteries should be helpful for a broad group of pathologists, from beginning pathology residents to experienced cardiovascular pathologists.

Chronic Stable Angina

By definition, chronic stable angina is angina that has been stable with regard to frequency and severity for at least 2 months. Chronic stable angina is the initial manifestation of coronary heart disease in approximately 50% of patients. Typically, this type of angina occurs in the setting of atherosclerotic coronary arterial narrowing, although other causes are possible. This review covers the epidemiology, pathophysiology, initial evaluation, differential diagnosis, management, and treatment of patients with chronic stable angina. Figures show noninvasive testing and the probability of coronary artery disease; diagnosis of patients with suspected ischemic heart disease; probability of severe coronary artery disease; coronary outcomes for high- versus low-intensity statin therapy; optimal medical therapy (OMT) versus OMT and percutaneous coronary intervention for chronic angina; OMT versus percutaneous coronary intervention for stable coronary heart disease; and coronary artery bypass grafting versus percutaneous coronary intervention for diabetes and coronary artery disease. Tables list the grading of angina pectoris by the Canadian Cardiovascular Society classification system, the differential diagnosis of chest pain, conditions promoting myocardial oxygen supply and demand mismatch, the features of typical angina, the classification of chest pain, a comparison of the pretest likelihood of coronary heart disease (CHD) in low-risk and high-risk symptomatic patients, the posttest probability of significant CHD based on pretest probabilities of CHD and normal or abnormal results of noninvasive studies, survival according to risk groups based on Duke treadmill scores, high- and moderate-intensity statin therapy, revascularization to improve survival compared with medical therapy, revascularization to improve symptoms with significant anatomic (≥ 50% left main or ≥ 70% nonleft main coronary artery disease) or physiologic (fractional flow reserve ≤ 0.80) coronary artery stenoses, and questions recommended by an expert panel for patients with chronic stable angina at follow-up visits. This review contains 7 highly rendered figures, 13 tables, and 109 references.

Correlation between Angiographic and Physiologic Evaluation of Coronary Artery Narrowings in Patients With Aortic Valve Stenosis

We aimed to assess the correlation between angiographic and physiologic evaluation of coronary lesions in aortic stenosis (AS) patients presenting with intermediate coronary stenoses at the angiography. From 2002 to 2010, we included 163 patients from 2 centers with both AS and coronary artery disease (CAD), matched by age and gender with 163 contemporary patients with CAD alone. With both quantitative coronary angiography and fractional flow reserve (FFR), we assessed 259 coronary stenoses in the AS+ CAD group, and 256 in the CAD alone group. A significant correlation was found between diameter stenosis (DS) and FFR in both groups, although this was significantly stronger in the AS+ CAD than in the CAD alone group (R=-0.63 vs-0.44, p <0.01). Likewise, the correlation between minimum lumen diameter and FFR was stronger in the AS+ CAD than in the CAD alone group (R=-0.54 vs-0.41, p= 0.05). Receiver operator characteristic curves analysis showed that DS was a better predictor of hemodynamically significant coronary stenoses (FFR ≤0.8) in the AS+ CAD rather than in the CAD alone group (area under the curve= 0.83 vs 0.67, p <0.01). With 50% DS cut-off value, the sensitivity, specificity, and accuracy was 77%, 66%, and 70% in the AS+ CAD group versus 59%, 63%, and 61% in the CAD alone group. In both groups, the diagnostic accuracy of DS in predicting FFR was higher in the right and circumflex coronary artery compared with the left anterior descending artery (LAD), although this was only statistically significant in the AS+ CAD group (area under the curve 0.88 in the right and circumflex coronary artery vs 0.76 in LAD, p= 0.03). In conclusion, the correlation between the angiographic and hemodynamic significance of coronary stenoses is modest in AS patients. The assessment of CAD severity solely based on angiography poorly predicts the hemodynamic significance of the coronary stenosis especially when these are located in the LAD.

Full Development of Consequences of Congenital Pulmonic Stenosis in Eighty-Four Years

Described herein is an 84-year-old woman, the oldest reported, with severe pulmonic stenosis who underwent a highly successful pulmonic valvotomy at age 77 and highly unsuccessfully attempted percutaneous pulmonic valve implantation at age 84. During the 84years she developed nearly all clinical and morphologic consequences of pulmonic stenosis, including heavy calcification of the pulmonic valve, heavy calcification of the tricuspid valve annulus, severe right ventricular wall thickening without ventricular cavity dilation, aneurysm of the pulmonary truck, multiple focal ventricular wall scars without narrowing of the epicardial coronary arteries, wall thickening and luminal narrowing of the intramural coronary arteries, and extremely low 12-lead QRS electrocardiographic voltage.

Do we need invasive confirmation of cardiac magnetic resonance results?

IntroductionCoronary artery revascularization is indicated in patients with documented significant obstruction of coronary blood flow associated with a large area of myocardial ischemia and/or untreatable symptoms. There are a few invasive or noninvasive methods that can provide information about the functional results of coronary artery narrowing. The application of more than one method of ischemia detection in one patient to reevaluate the indications for revascularization is used in case of atypical or no symptoms and/or borderline stenosis.AimTo evaluate whether the results of cardiac magnetic resonance need to be reconfirmed by the invasive functional method.Material and methodsThe hospital database revealed 25 consecutive patients with 29 stenoses who underwent cardiac magnetic resonance (CMR) and fractional flow reserve (FFR) between the end of 2010 and the end of 2014. The maximal time interval between CMR and FFR was 6 months. None of the patients experienced any clinical events or underwent procedures on coronary arteries between the studies.ResultsAccording to the analysis, the agreement of CMR perfusion with the FFR method was at the level of 89.7%. Assuming that FFR is the gold standard in assessing the severity of stenoses, the sensitivity of CMR perfusion was 90.9%. The percentage of non-severe lesions which were correctly identified in CMR was 88.9%.ConclusionsThe study shows that CMR perfusion is a highly sensitive method to detect hemodynamically significant CAD and exclude nonsevere lesions. With FFR as the reference standard, the diagnostic accuracy of MR perfusion to detect ischemic CAD is high.

Characteristics, circumstances and pathology of sudden or unnatural deaths of cases with evidence of pathological hoarding

The study aimed to determine the characteristics and circumstances of cases sudden or unnatural death (n = 61) with evidence of pathological hoarding, their major organ pathology and toxicology. The mean age was 65·8 yrs (a mean of 16.1 years of potential life lost), 62·3% were male, and 28·2% were obese. 95·1% lived alone, and 96·7% died in their residence, with no medical intervention. In all cases severe squalor and extensive hoarding were noted. The direct cause of death was attributed to disease in 75·4%, heart disease being a significant factor in 52·5%. Accidents causing death directly related to hoarding occurred in two cases. Autopsy revealed extensive pathology: severe coronary artery narrowing (42·4%), myocardial replacement fibrosis (44·1%), emphysema (39·0%), nephrosclerosis (46·6%). Signs of hypothermia were present in 14·8%, and diabetes was diagnosed in 21·3%. The most commonly detected substance was alcohol (32·1%). Medications for heart disease (5·4%) or diabetes (7·1%) were rare. The overall clinical picture was of an isolated group, with a heavy burden of physical disease and, in all probability, a high level of psychiatric disorders, who died alone in their homes.

Feasibility of omitting provocation test with 50μg of acetylcholine in left coronary artery.

According to the Japanese Circulation Society guideline of vasospastic angina, incremental doses of acetylcholine (ACh) are prescribed for coronary spasm provocation: 20 and 50μg for the right coronary artery (RCA), and 20, 50 and 100μg for the left coronary artery (LCA). However, provocation by low doses of ACh in patients with low vasoreactivity may be less needed, and the requirement of 50μg of ACh for the LCA in these patients has not been evaluated. In the present study, patients who underwent ACh provocation test for both the RCA and LCA were included. The positive diagnosis of intracoronary ACh provocation test was defined as total or subtotal coronary artery narrowing (i.e., angiographic coronary artery spasm) accompanied by chest pain and/or ischemic electrocardiographic changes. Coronary artery constriction was visually evaluated and defined as coronary artery diameter reduction <25 or 25-90% in patients without angiographic coronary artery spasm by 20µg of ACh in the LCA. There were 33 out of 249 patients (13%) with LCA spasm by 20µg of ACh. In subjects without LCA spasm by 20µg of ACh, patients with coronary constriction <25% (n=101) by 20µg of ACh in the LCA rarely showed coronary artery spasm induced by 50μg of ACh in the LCA, in comparison to those with coronary constriction 25-90% (n=115) (2.6 vs. 32.7%, p<0.001). None of the patients with coronary constriction <25% by 20µg of ACh in the LCA had cardiac complications associated with administration of ACh. In conclusion, omission of 50µg of ACh in the LCA may be possible when there is little coronary artery constriction by 20µg of ACh in the LCA during provocation test, leading to less contrast and shortens overall procedure time.

Impact of old age on clinical and angiographic characteristics of coronary artery spasm as assessed by acetylcholine provocation test.

BackgroundSmoking and other risk factors have been well known as important factors of variant angina or coronary artery spasm (CAS). However, clinical features related to age on coronary artery spasm have been rarely evaluated.MethodsWe evaluated 3155 consecutive patients with insignificant coronary artery lesion. Patients underwent Acetylcholine (Ach) provocation test for induction of CAS. CAS was defined as > 70% luminal narrowing of coronary arteries during Ach provocation test. The results of Ach provocation test were compared among age groups; < 45 years (Group 1), 45–54 years (Group 2), 55–64 years (Group 3), and ≥ 65 years (Group 4).ResultsOlder patients had higher incidence of hypertension, diabetes, but lower incidence rate of current smoking, male sex compared with younger patients. Positive Ach provocation test finding was frequently showed with aging (47.36% vs. 58.3% vs. 62.6% vs. 61.5%; P < 0.001). Multivariate logistic analysis showed that age, male, and myocardial bridge were independent predictors of CAS induced by Ach provocation test.ConclusionOur present study showed that old age was independent predictor for Ach-induced significant coronary artery spasm.

Mental activity in different semantic contexts has EEG correlates in 10-13 Hz frequency band

Coronary artery disease (CAD) is the narrowing of coronary arteries leading to inadequate supply of nutrients and oxygen to the heart muscles. Over time, the condition can weaken the heart muscles and may lead to heart failure, arrhythmias and even sudden cardiac death. Hence, the early diagnosis of CAD can save life and prevent the risk of stroke. Electrocardiogram (ECG) depicts the state of the heart and can be used to detect the CAD. Small changes in the ECG signal indicate a particular disease. It is very difficult to decipher these minute changes in the ECG signal, as it is prone to artifacts and noise. Hence, we detect the R peaks from the ECG and use heart rate signals for our analysis. The manual inspection of the heart rate signals is time consuming, taxing and prone to errors due to fatigue. Hence, a decision support system independent of human intervention can yield accurate repeatable results. In this paper, we present a new method for diagnosis of CAD using tunable-Q wavelet transform (TQWT) based features extracted from heart rate signals. The heart rate signals are decomposed into various sub-bands using TQWT for better diagnostic feature extraction. The nonlinear feature called centered correntropy (CC) is computed on decomposed detail sub-band. Then the principal component analysis (PCA) is performed on these CC to transform the number of features. These clinically significant features are subjected to least squares support vector machine (LS-SVM) with different kernel functions for automated diagnosis. The experimental results demonstrate better classification accuracy, sensitivity, specificity and Matthews correlation coefficient using Morlet wavelet kernel function with optimized kernel and regularization parameters. Also, we have developed a novel CAD Risk index using significant features to discriminate the two classes using a single number. Our proposed methodology is more suitable in classification of normal and CAD heart rate signals and can aid the clinicians while screening the CAD patients.

Deaths in triathletes: immersion pulmonary oedema as a possible cause.

Background/aimTo address the question as to whether immersion pulmonary oedema (IPO) may be a common cause of death in triathlons, markers of swimming-induced pulmonary oedema (SIPO) susceptibility were sought in triathletes' postmortem examinations.MethodsDeaths while training for or during triathlon events in the USA and Canada from October 2008 to November 2015 were identified, and postmortem reports requested. We assessed obvious causes of death; the prevalence of left ventricular hypertrophy (LVH); comparison with healthy triathletes.ResultsWe identified 58 deaths during the time period of the review, 42 (72.4%) of which occurred during a swim. Of these, 23 postmortem reports were obtained. Five individuals had significant (≥70%) coronary artery narrowing; one each had coronary stents; retroperitoneal haemorrhage; or aortic dissection. 9 of 20 (45%) with reported heart mass exceeded 95th centile values. LV free wall and septal thickness were reported in 14 and 9 cases, respectively; of these, 6 (42.9%) and 4 (44.4%) cases exceeded normal values. 6 of 15 individuals (40%) without an obvious cause of death had excessive heart mass. The proportion of individuals with LVH exceeded the prevalence in the general triathlete population.ConclusionsLVH—a marker of SIPO susceptibility—was present in a greater than the expected proportion of triathletes who died during the swim portion. We propose that IPO may be a significant aetiology of death during the swimming phase in triathletes. The importance of testing for LVH in triathletes as a predictor of adverse outcomes should be explored further.

Effect of Fractional Flow Reserve (≤0.90 vs >0.90) on Long-Term Outcome (>10 Years) in Patients With Nonsignificant Coronary Arterial Narrowings

We assessed the long-term (>10years) clinical course of patients with documented coronary lesions deemed nonsignificant according to fractional flow reserve (FFR) assessment and investigated whether the initial FFR value impacted on prognosis. From January 2000 to October 2003, all patients submitted to coronary angiography with FFR measurement were included in a single-center, prospective registry. Patients with an FFR value >0.80 were treated medically without revascularization. Major adverse cardiac events (MACE) (death, acute coronary syndrome (ACS), or coronary revascularization) were compared according to initial FFR value (absolute value and by category, ≤0.90 vs >0.90). Analyses were performed using a multivariable Cox model and propensity score matching. Among 257 patients (332 lesions) treated medically initially, 131 (51%, 143 lesions) had FFR ≤0.90 and 126 (49%, 189 lesions) >0.90. During follow-up (median duration, 11.6years), 82 (31.9%) had a MACE, 38 (14.8%) died, 17 (6.6%) had ACS, 93 (36.2%) had repeat coronary angiography, and 27 (10.5%) had revascularization. There was no clinical, biologic or angiographic difference between patients with initial FFR value ≤0.90 versus >0.90. Adjusted Cox model showed no difference in relative risk of MACE, death, ACS, or revascularization. Coronary angiographies were numerically more frequent in patients with FFR ≤0.90, versus FFR >0.90. These findings were confirmed by propensity score-matched comparison. In patients with coronary narrowings left unrevascularized based on FFR, an FFR value between 0.80 and 0.90 has no impact on long-term outcome compared with those with FFR >0.90. In conclusion, patients with high FFR values should not be considered as having a lower risk of coronary event.