Older Adults at Risk for Atrial Fibrillation Lack Knowledge and Confidence to Seek Treatment for Signs and Symptoms.

Early detection of atrial fibrillation (AF) is crucial for averting AF-related stroke and heart failure, but treatment is delayed when AF is not recognized. The critical need for early detection and treatment requires education to promote AF awareness. Knowledge deficits, attitudes, and beliefs about AF that should be addressed to improve awareness and reduce treatment-seeking delay in older adults at risk for developing AF have not been well documented. The purpose of this study was to describe knowledge, treatment-seeking attitudes, and beliefs about AF in adults ⩾ 65 years old and identify demographic characteristics associated with knowledge, attitudes, and beliefs. Patients with no history of AF recruited from an academic medical center were interviewed using the Knowledge, Attitudes, and Beliefs about Atrial Fibrillation Survey. Data were analyzed using descriptive statistics and independent t tests. Participants (N = 180) were 63% male with a mean age of ±3.± 6.0 years, and 52% held ⩾ 4-year college degree. About one third could not identify common symptoms of AF including palpitations (31%), chest pain (36%), dyspnea (30%), and fatigue (35%). A majority (84%) lacked confidence to recognize AF, and 58% were not sure when they should seek care for AF symptoms. Nearly a third (32%) believed palpitations are always present with AF, and 74% believed that low energy would not be their only symptom of AF. Higher scores for AF Symptom Knowledge (p = .02) were observed in females, and General Knowledge about AF was greater for younger participants (p < .001). Participants lacked knowledge and confidence to aid decision-making for treatment-seeking for symptoms of AF and held inaccurate beliefs about AF that could hinder early treatment-seeking. Programs to promote AF awareness should explain the spectrum of symptoms that may be manifested by AF and include action plans for responding to symptoms

What's the Risk? Older Women Report Fewer Symptoms for Suspected Acute Coronary Syndrome than Younger Women.

The purpose of the study was to determine whether older (≥65 years) and younger (<65 years) women presenting to the emergency department (ED) with symptoms suggestive of acute coronary syndrome (ACS) varied on risk factors, comorbid conditions, functional status, and symptoms that have implications for emergent cardiac care. Women admitted to five EDs were enrolled. The ACS Symptom Checklist was used to measure symptoms. Comorbid conditions and functional status were measured with the Charlson Comorbidity Index and Duke Activity Status Index. Logistic regression models were used to evaluate symptom differences in older and younger women adjusting for ACS diagnosis, functional status, body mass index (BMI), and comorbid conditions. Analyses were stratified by age, and interaction of symptom by age was tested. Four hundred women were enrolled. Mean age was 61.3 years (range 21-98). Older women (n = 163) were more likely to have hypertension, hypercholesterolemia, never smoked, lower BMI, more comorbid conditions, and lower functional status. Younger women (n = 237) were more likely to be members of minority groups, be college-educated, and have a non-ACS discharge diagnosis. Younger women had higher odds of experiencing chest discomfort, chest pain, chest pressure, shortness of breath, nausea, sweating, and palpitations. Lack of chest symptoms and shortness of breath (key symptoms triggering a decision to seek emergency care) may cause older women to delay seeking treatment, placing them at risk for poorer outcomes. Younger African American women may require more comprehensive risk reduction strategies and symptom management

ESC core curriculum for the general cardiologist (2013)

[No abstract available

Cardiotoxicity with vascular endothelial growth factor inhibitor therapy

Angiogenesis inhibitors targeting the vascular endothelial growth factor (VEGF) signaling pathway (VSP) have been important additions in the therapy of various cancers, especially renal cell carcinoma and colorectal cancer. Bevazicumab, the first VSP to receive FDA approval in 2004 targeting all circulating isoforms of VEGF-A, has become one of the best-selling drugs of all times. The second wave of tyrosine kinase inhibitors (TKIs), which target the intracellular site of VEGF receptor kinases, began with the approval of sorafenib in 2005 and sunitinib in 2006. Heart failure was subsequently noted, in 2–4% of patients on bevacizumab and in 3–8% of patients on VSP-TKIs. The very fact that the single-targeted monoclonal antibody bevacizumab can induce cardiotoxicity supports a pathomechanistic role for the VSP and the postulate of the “vascular” nature of VSP inhibitor cardiotoxicity. In this review we will outline this scenario in greater detail, reflecting on hypertension and coronary artery disease as risk factors for VSP inhibitor cardiotoxicity, but also similarities with peripartum and diabetic cardiomyopathy. This leads to the concept that any preexisting or coexisting condition that reduces the vascular reserve or utilizes the vascular reserve for compensatory purposes may pose a risk factor for cardiotoxicity with VSP inhibitors. These conditions need to be carefully considered in cancer patients who are to undergo VSP inhibitor therapy. Such vigilance is not to exclude patients from such prognostically extremely important therapy but to understand the continuum and to recognize and react to any cardiotoxicity dynamics early on for superior overall outcomes

Causes of prehospital misinterpretations of ST elevation myocardial infarction

Objectives: To determine the causes of software misinterpretation of ST elevation myocardial infarction (STEMI) compared to clinically identified STEMI to identify opportunities to improve prehospital STEMI identification. Methods: We compared ECGs acquired from July 2011 through June 2012 using the LIFEPAK 15 on adult patients transported by the Los Angeles Fire Department. Cases included patients ≥18 years who received a prehospital ECG. Software interpretation of the ECG (STEMI or not) was compared with data in the regional EMS registry to classify the interpretation as true positive (TP), true negative (TN), false positive (FP), or false negative (FN). For cases where classification was not possible using registry data, 3 blinded cardiologists interpreted the ECG. Each discordance was subsequently reviewed to determine the likely cause of misclassification. The cardiologists independently reviewed a sample of these discordant ECGs and the causes of misclassification were updated in an iterative fashion. Results: Of 44,611 cases, 50% were male (median age 65; inter-quartile range 52–80). Cases were classified as 482 (1.1%) TP, 711 (1.6%) FP, 43371 (97.2%) TN, and 47 (0.11%) FN. Of the 711 classified as FP, 126 (18%) were considered appropriate for, though did not undergo, emergent coronary angiography, because the ECG showed definite (52 cases) or borderline (65 cases) ischemic ST elevation, a STEMI equivalent (5 cases) or ST-elevation due to vasospasm (4 cases). The sensitivity was 92.8% [95% CI 90.6, 94.7%] and the specificity 98.7% [95% CI 98.6, 98.8%]. The leading causes of FP were ECG artifact (20%), early repolarization (16%), probable pericarditis/myocarditis (13%), indeterminate (12%), left ventricular hypertrophy (8%), and right bundle branch block (5%). There were 18 additional reasons for FP interpretation (<4% each). The leading causes of FN were borderline ST-segment elevations less than the algorithm threshold (40%) and tall T waves reducing the ST/T ratio below threshold (15%). There were 11 additional reasons for FN interpretation occurring ≤3 times each. Conclusion: The leading causes of FP automated interpretation of STEMI were ECG artifact and non-ischemic causes of ST-segment elevation. FN were rare and were related to ST-segment elevation or ST/T ratio that did not meet the software algorithm threshold

Biomarkers of Inflammation and Fibrosis in Kawasaki Disease Patients Years After Initial Presentation With Low Ejection Fraction.

Background Coronary artery aneurysms and myocarditis are well-recognized complications of Kawasaki disease (KD) but no systematic evaluation of the consequences of myocarditis has been performed in the subset presenting with low ejection fraction (EF). We postulated that more severe myocardial inflammation as evidenced by low EF during the acute phase could lead to late myocardial fibrosis. Methods and Results We measured the carboxyterminal propeptide of procollagen type I (PIPC), soluble suppressor of tumorigenicity 2, galectin-3 (Gal-3), growth-differentiation factor-15, and calprotectin by ELISA in late convalescent blood samples from 16 KD patients who had an EF ≤55% on their initial echocardiogram. Results were compared with samples from sex- and age-matched KD patients with initial EF >60%. In the univariate analysis, the median Gal-3 and PIPC levels in the low EF group were significantly higher than those in the normal EF group (Gal-3: low EF 6.216 versus normal EF 4.976 mg/dL P=0.038, PIPC: low EF 427.4 versus normal EF 265.2 mg/dL, P=0.01). In a multivariable analysis, there were significant differences for Gal-3 and PIPC levels between the low and normal EF groups, adjusting for age, sex, and worst z score. Conclusions Convalescent KD patients with a history of low EF during the acute illness had significantly elevated levels of Gal-3 and PIPC when compared with matched-control KD patients with normal EF. These findings raise concern for myocardial fibrosis as a potential late sequela of the more severe myocarditis experienced by a subset of KD patients during the acute phase

Determining predictors of underlying etiology and clinical deterioration in patients with physiologic instability in the emergency department

Thesis (M.A.)--Boston UniversityShock is a critical state defined by inadequate oxygen delivery to tissues. It is well known in the critical care community that early diagnosis and treatment of shock are crucial to improving patient outcomes. However, in many cases, when a state of circulatory shock has been reached, irreversible damage already occurred. In the present study, we broadened our patient cohort from those with shock to those with physiologic instability with the intent of finding predictive factors that allow us to recognize when a patient is at risk for deterioration or when it is already occurring. These patients included patients with pre-shock, shock, and other forms of dysfunction. The purpose of this study was to determine the predictors of underlying etiology of physiologic instability as well as the likelihood of clinical deterioration in these various states, using elements from the physical exam, history, laboratory values, and vital sign measurements. This study was a prospective observational study of patients, from November 15, 2012 to March 1, 2013, found to have physiologic instability in the emergency department at an urban, academic tertiary-care hospital with 55,000 annual visits. Physiologic instability was defined as any one of the following abnormalities: heart rate (HR) > 130, respiratory rate (RR>24), shock index (SI) > 1, systolic blood pressure (SBP) 4.0 mmol/L, for a time period of more than five minutes. We identified 540 patients, 74.8% of which were included. Data describing epidemiology, and elements from the patient history and physical exam were abstracted from physician charts and the final etiology of physiologic instability, defined as septic, cardiogenic, hypovolemic, hemorrhagic, or other, was adjudicated by a physician. Blood samples from a subset of our patient group were collected from the hospital hematology laboratory and sent to the Wyss Institute to be analyzed using a novel bacterial detection assay. All of the covariates that data was collected for were analyzed to determine their diagnostic and prognostic value. [TRUNCATED

Cardiac manifestations of PRKAG2 mutation.

BACKGROUND:The Protein Kinase AMP-Activated Non-Catalytic Subunit Gamma 2 (PRKAG2) cardiac syndrome is characterized by glycogen accumulation in the cardiac tissue. The disease presents clinically with hypertrophic cardiomyopathy (HCM), and it is often associated with conduction abnormalities. CASE PRESENTATION:A 23 year-old female with history of Wolff-Parkinson-White (WPW) and HCM presented for evaluation after an episode of Non-ST Elevation Myocardial Infarction (NSTEMI). The patient was found to have severe coronary bridging on angiography and underwent an unroofing of the left anterior descending artery (LAD). Due to the constellation of symptoms, the patient underwent genetic testing and a cardiac muscle biopsy. Genetic testing was significant for an Arg302Gln mutation in the PRKAG2 gene. Cardiac tissue biopsy revealed significant myocyte hypertrophy and large vacuoles with glycogen stores. CONCLUSION:The pathologic and genetics findings of our patient are consistent with PRKAG2 syndrome. Patients presenting with conduction abnormalities and suspected HCM should be considered for genetic testing to identify possible underlying genetic etiologies

Surviving to acute myocardial infarction: The role of psychological factors and alexithymia in delayed time to searching care: A systematic review

The time from symptom onset to reperfusion is a critical determinant of myocardial salvage and clinical outcomes in patients with acute myocardial infarction (AMI). This time period could be delayed if people do not seek help promptly and/or if the health system is not efficient in responding quickly and attending to these individuals. The aim of this study was to identify psychological factors associated with pre-hospital delay (PHD) or patients’ decisional delay (PDD) in people with an ongoing AMI. A search in PubMed/Medline from 1990 to 2021 with the keywords “pre-hospital delay” OR “prehospital delay” OR “patient delay” OR “decisional delay” OR “care seeking behavior” AND “psychological factors” OR “alexithymia” AND “myocardial infarction” was performed. Thirty-six studies were included, involving 10.389 patients. Wrong appraisal, interpretation and causal beliefs about symptoms, denial of the severity of the symptoms and high levels of alexithymia were found related to longer PHD or PDD. Alexithymia may be an overarching construct that explains the disparate findings of the studies exploring the role of psychological factors in PHD or PDD. Further studies are needed in order to analyse the role of alexithymia in patients with risk factors for AMI to prevent delay

The Health Disparities Myth

Many experts today insist that bias in the doctor's office will lead to poorer treatment of minority patients. A new monograph by Jonathan Klick of Florida State University and AEI's Sally Satel, The Health Disparities Myth: Diagnosing the Treatment Gap (AEI Press, 2006) found no evidence to support the idea that racially biased doctors are a cause of poor minority health