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Aims Stress echocardiography is widely used to identify obstructive coronary artery disease (CAD). High accuracy is reported in expert hands but is dependent on operator training and image quality. The EVAREST study provides UK-wide data to evaluate real-world performance and accuracy of stress echocardiography. Methods and results Participants undergoing stress echocardiography for CAD were recruited from 31 hospitals. Participants were followed up through health records which underwent expert adjudication. Cardiac outcome was defined as anatomically or functionally significant stenosis on angiography, revascularization, medical management of ischaemia, acute coronary syndrome, or cardiac-related death within 6 months. A total of 5131 patients (55% male) participated with a median age of 65 years (interquartile range 57–74). 72.9% of studies used dobutamine and 68.5% were contrast studies. Inducible ischaemia was present in 19.3% of scans. Sensitivity and specificity for prediction of a cardiac outcome were 95.4% and 96.0%, respectively, with an accuracy of 95.9%. Sub-group analysis revealed high levels of predictive accuracy across a wide range of patient and protocol sub-groups, with the presence of a resting regional wall motion abnormalitiy significantly reducing the performance of both dobutamine (P Conclusion Stress echocardiography has high accuracy across UK-based hospitals and thus indicates stress echocardiography is being delivered effectively in real-world practice, reinforcing its role as a first-line investigation in the assessment of patients with stable chest pain.

This chapter will cover in detail the two-dimensional sonoanatomy and pathophysiology of common aortic valve lesions and explain step by step how to image the aortic valve and detect significant disease. The advanced section will introduce how to use colour and spectral Doppler to recognize acute and severe pathology that requires immediate management.

A 50-year-old Asian man presented to the emergency department with chest pain. On arrival he suffered a cardiac arrest with ventricular fibrillation from which he was successfully resuscitated. A post-resuscitation ECG showed right bundle branch block with inferior ST elevation, and he was immediately transferred for primary percutaneous coronary intervention. Right femoral arterial access was obtained and blood pressure was noted to be 140/30 mm Hg. Coronary angiography showed mild atherosclerosis in the left anterior descending and circumflex arteries. On attempted catheter intubation of the right coronary artery (figure 1A), contrast extravasation was noted (asterisk). An aortogram was conducted (figure 1B). Figure 1 (A) Attempted coronary angiography of the right coronary artery. (B) Aortogram. What is the most likely diagnosis? 1. Catheter-induced …

The enzyme neutral endopeptidase (NEP; EC 3.4.24.11) cleaves several vasoactive peptides such as the atrial natriuretic peptide (ANP). ANP is a hormone of cardiac origin with diuretic and natriuretic actions. Despite elevated circulating levels of ANP, congestive heart failure (CHF) is characterized by progressive sodium and water retention. In order to elucidate the loss of natriuretic and diuretic properties of ANP in CHF we analyzed activity, protein concentrations, mRNA and immunostaining of NEP in kidneys of different models of severe CHF in the rat.CHF was induced by either aortocaval shunt, aortic banding or myocardial infarction in the rat. All models were defined by increased left ventricular end-diastolic pressure and decreased contractility. The diminished effectiveness of ANP was reflected by reduced cGMP/ANP ratio in animals with shunt or infarction. Renal NEP activity was increased in rats with aortocaval shunt (203 +/- 7%, p < 0.001), aortic banding (184 +/- 11%, p < 0.001) and infarction (149 +/- 10%, p < 0.005). Western blot analysis revealed a significant increase in renal NEP protein content in two models of CHF (shunt: 214 +/- 57%, p < 0.05; infarction: 310 +/- 53 %, p < 0.01). The elevated protein expression was paralleled by a threefold increase in renal NEP-mRNA level in the infarction model. The increased renal NEP protein expression and activity may lead to enhanced degradation of ANP and may contribute to the decreased renal response to ANP in heart failure. Thus, the capacity to counteract sodium and water retention, would be diminished. The increased renal NEP activity may therefore be a hitherto unknown factor in the progression of CHF.

Objective: Recently, deletion of specific genes by so called knock-out techniques has become important for investigating the pathogenesis of various diseases. This form of genetic engineering is widely performed in murine models. There are, however, only a limited number of mouse models available in cardiovascular pathology. The objective of this study, therefore, was to develop a new model of overt congestive heart failure associated with myocardial hypertrophy in the mouse. Methods: Female C57/BL6 mice weighing 19–20 g were anesthetized with ether. After abdominal incision, the aorta was temporarily clamped proximal to the renal arteries. The aorta was then punctured with a needle (outer diameter 0.6 mm) and the needle was further advanced into the adjacent vena cava. After withdrawal of the needle, the aortic puncture site was sealed with cyanoacrylate glue. The clamp was removed, and the patency of the shunt was visually verified as swelling and mixing of venous and arterial blood in the vena cava. Sham-operated mice served as controls. Results: Perioperative mortality of mice with aortocaval shunt was 42%. Four weeks after shunt induction, mice showed a significant cardiac hypertrophy with a relative heart weight of 7.5 ± 0.2 mg/100 g body weight (vs. 5.1 ± 0.7 mg/100 g in control mice, P < 0.001). While no changes in blood pressure and heart rate occurred, left ventricular enddiastolic pressure was significantly increased in mice with shunt, and left ventricular contractility was impaired from 6331 ± 412 to 4170 ± 296 mmHg/s (P < 0.05). Plasma concentrations of atrial natriuretic peptide (ANP) and its second messenger cGMP as humoral markers of heart failure as well as ventricular expression of ANP - and brain natriuretic peptide (BNP)-mRNA were significantly increased in mice with shunt compared to control mice. Conclusions: The aortocaval shunt in the mouse constitutes a new model of overt congestive heart failure with impaired hemodynamic parameters and may be a useful tool to investigate the role of particular genes in the development of heart failure.

We report the case of a 47-year-old man who presented with several episodes of left precordial pain, one of which had been severe, but was unrelated to exertion or posture. Transthoracic echocardiography and cardiovascular magnetic resonance showed evidence of congenital partial absence of the left pericardium and severe tricuspid regurgitation. Both diagnoses were confirmed at surgery when the pericardial defect was repaired and the tricuspid valve was replaced at the same operation. He went on to make a good recovery.

A 45-year-old male was admitted to the hospital with recurrent, stabbing, nonexertional chest pain. Chest x-ray showed an increased cardiothoracic ratio (Figure 1A), and ECG demonstrated sinus rhythm with incomplete right bundle-branch block and poor R-wave progression (Figure 1B). Echocardiography showed normal left ventricular dimensions and function; however, the right ventricle appeared grossly dilated with moderate to severe tricuspid regurgitation with no evidence of intracardiac shunts. These findings were confirmed by right heart catheterization, which also showed normal pulmonary and right atrial pressures without a pressure gradient over the pulmonic valve. Catheterization of the left heart showed normal ventricular pressures and function as well as normal coronary arteries. The patient was referred for cardiac magnetic resonance imaging (CMR) with suspected right ventricular cardiomyopathy. CMR showed cardiac displacement into the left hemithorax (Figure 2A). There was severe tricuspid regurgitation with marked dilatation of both the right atrium (6×8 cm) and ventricle (end-diastolic volume, 343 mL). Right ventricular function was mildly reduced (ejection fraction, 46%) without localized wall motion abnormalities. Left ventricular volumes and …

Background— Chronic heart failure (CHF) is a major cause of morbidity and mortality that requires a novel approach to therapy. Perhexiline is an antianginal drug that augments glucose metabolism by blocking muscle mitochondrial free fatty acid uptake, thereby increasing metabolic efficiency. We assessed the effects of perhexiline treatment in CHF patients. Methods and Results— In a double-blind fashion, we randomly assigned patients with optimally medicated CHF to either perhexiline (n=28) or placebo (n=28). The primary end point was peak exercise oxygen consumption (V̇ o 2 max), an important prognostic marker. In addition, the effect of perhexiline on myocardial function and quality of life was assessed. Quantitative stress echocardiography with tissue Doppler measurements was used to assess regional myocardial function in patients with ischemic CHF. 31 P magnetic resonance spectroscopy was used to assess the effect of perhexiline on skeletal muscle energetics in patients with nonischemic CHF. Treatment with perhexiline led to significant improvements in V̇ o 2 max (16.1±0.6 to 18.8±1.1 mL · kg −1 · min −1 ; P P =0.04), and left ventricular ejection fraction (24±1% to 34±2%; P Conclusions— In patients with CHF, metabolic modulation with perhexiline improved V̇ o 2 max, left ventricular ejection fraction, symptoms, resting and peak stress myocardial function, and skeletal muscle energetics. Perhexiline may therefore represent a novel treatment for CHF with a good safety profile, provided that the dosage is adjusted according to plasma levels.

Background— It is well known that patients with type 2 diabetes have increased risk of cardiovascular disease, but it is not known whether they have underlying abnormalities in cardiac or skeletal muscle high-energy phosphate metabolism. Methods and Results— We studied 21 patients with type 2 diabetes with no evidence of coronary artery disease or impaired cardiac function, as determined by echocardiography, and 15 age-, sex-, and body mass index-matched control subjects. Cardiac high-energy phosphate metabolites were measured at rest using 31 P nuclear magnetic resonance spectroscopy (MRS). Skeletal muscle high-energy phosphate metabolites, intracellular pH, and oxygenation were measured using 31 P MRS and near infrared spectrophotometry, respectively, before, during, and after exercise. Although their cardiac morphology, mass, and function appeared to be normal, the patients with diabetes had significantly lower phosphocreatine (PCr)/ATP ratios, at 1.50±0.11, than the healthy volunteers, at 2.30±0.12. The cardiac PCr/ATP ratios correlated negatively with the fasting plasma free fatty acid concentrations. Although skeletal muscle energetics and pH were normal at rest, PCr loss and pH decrease were significantly faster during exercise in the patients with diabetes, who had lower exercise tolerance. After exercise, PCr recovery was slower in the patients with diabetes and correlated with tissue reoxygenation times. The exercise times correlated negatively with the deoxygenation rates and the hemoglobin (Hb)A 1c levels and the reoxygenation times correlated positively with the HbA 1c levels. Conclusions— Type 2 diabetic patients with apparently normal cardiac function have impaired myocardial and skeletal muscle energy metabolism related to changes in circulating metabolic substrates.