Myocardial Ischemia

In end-stage heart failure (HF) that is not eligible for mechanical assist device or heart transplant, palliative care serves to maximise symptom control and quality of life. We sought to evaluate the impact of home-based advance care programme (ACP) on healthcare utilisation in end-stage HF patients. Prospectively collected registry data on all end-stage HF recruited into ACP between July 2008 and July 2010 were analysed. Chart reviews were conducted on HF database and hospital electronic records. Phone interview and home visit details by ACP team were extracted to complete data entry. HF and all-cause hospitalisations 1 year before, and any time after ACP inception were defined as events. For the latter analysis, follow-up duration adjustment to event episodes was performed to account for death less than a year. Forty-four patients (mean age 79 years, 39% men) were followed up for 15±8 months. Fifty-seven percent had diabetes, 80% ischaemic heart disease, and 60% chronic kidney di...

Cardiovascular complications of cocaine abuse include myocardial ischemia and infarction, dysrhythmias, cardiomyopathies and aortic dissection. The case in point pertains to a 26-year-old, Caucasian male, substance abuser who suffered a thoracic aortic dissection following the use of crack cocaine. The autopsy and histological findings showed a connective tissue abnormality including a focal microcystic medial necrosis and a fragmentation of the elastic fibers in the arterial walls. Blood concentrations of cocaine and benzoylecgonine, taken individually, were considered to be within a potentially toxic range. Blood concentrations of methadone also indicated use of this drug at the same time. The small amounts of morphine found in the blood and urine were compatible with heroine or morphine use more than 24 h before death.

Increasing numbers of elderly patients with severe co-existing medical diseases undergo major surgery. With these patients there is also an accompanying risk of age-related cardiovascular complications such as life-threatening myocardial ischaemia. We present a patient who suffered a myocardial infarction after a hemicolectomy and suffered a cardiac arrest in the recovery room. The therapeutic options available (e.g. coronary artery bypass grafting, acute percutaneous coronary angioplasty and peri-operative thrombolysis) are discussed and the successful management of the case by coronary angioplasty and stent implantation is described.

Magnetocardiography (MCG) is a non-invasive and risk-free technique allowing body surface recording of the magnetic fields generated by the electrical activity of the heart. The MCG recording system allows spatially and temporally accurate measurements of the very weak magnetic fields produced by currents flowing within myocardial fibers during cardiac activity. MCG has now been around for over 30 years, but only recently has progress in instrumentation put the technique on the verge of clinical applicability. This review summarizes the physical principles, instrumentation, main clinical applications and perspectives for the clinical use of MCG. This second part is devoted to the description of the main current clinical applications and perspectives.

BACKGROUND Assessment of health-related quality of life is widely recommended by European health agencies in relevant research studies as well as in clinical care. AIMS To validate the French version of the MacNew heart disease health-related quality of life questionnaire. METHODS As part of the International HeartQoL Project, 323 French-speaking patients with ischaemic heart disease (angina, n=76; myocardial infarction [MI], n=155; heart failure, n=91; mean age 58.6±11.3 years) were recruited at seven cardiac rehabilitation centres. All patients completed the French versions of the MacNew questionnaire, the Short Form-36 Health Survey (SF-36) and the Hospital Anxiety and Depression Scale, to evaluate the psychometric properties of the French version of the MacNew instrument. RESULTS The mean MacNew global scale scores were 4.6±0.8, 5.0±1.0 and 4.8±0.9 in patients with angina, MI and heart failure, respectively (P<0.05, MI versus angina). We observed minimal missing items and cei...

Abstract: Several experimental studies have shown that levocarnitine reduces myocardial injury after ischemia and reperfusion by counteracting the toxic effect of high levels of free fatty acids, which occur in ischemia, and by improving carbohydrate metabolism. In addition to increasing the rate of fatty acid transport into mitochondria, levocarnitine reduces the intramitochondrial ratio of acetyl-CoA to free CoA, thus stimulating the activity of pyruvate dehydrogenase and increasing the oxidation of pyruvate. Supplementation of the myocardium with levocarnitine results in an increased tissue carnitine content, a prevention of the loss of high-energy phosphate stores, ischemic injury, and improved heart recovery on reperfusion. Clinically, levocarnitine has been shown to have anti-ischemic properties. In small short-term studies, levocarnitine acts as an antianginal agent that reduces ST segment depression and left ventricular end-diastolic pressure. These short-term studies also show that levocarnitine releases the lactate of coronary artery disease patients subjected to either exercise testing or atrial pacing. These cardioprotective effects have been confirmed during aortocoronary bypass grafting and acute myocardial infarction. In a randomized multicenter trial performed on 472 patients, levocarnitine treatment (9 g/day by intravenous infusion for 5 initial days and 6 g/day orally for the next 12 months), when initiated early after acute myocardial infarction, attenuated left ventricular dilatation and prevented ventricular remodeling. In treated patients, there was a trend towards a reduction in the combined incidence of death and CHF after discharge. Levocarnitine could improve ischemia and reperfusion by (1) preventing the accumulation of long-chain acyl-CoA, which facilitates the production of free radicals by damaged mitochondria; (2) improving repair mechanisms for oxidative-induced damage to membrane phospholipids; (3) inhibiting malignancy arrhythmias because of accumulation within the myocardium of long-chain acyl-CoA; and (4) reducing the ischemia-induced apoptosis and the consequent remodeling of the left ventricle. Propionyl-l-carnitine is a carnitine derivative that has a high affinity for muscular carnitine transferase, and it increases cellular carnitine content, thereby allowing free fatty acid transport into the mitochondria. Moreover, propionyl-l-carnitine stimulates a better efficiency of the Krebs cycle during hypoxia by providing it with a very easily usable substrate, propionate, which is rapidly transformed into succinate without energy consumption (anaplerotic pathway). Alone, propionate cannot be administered to patients in view of its toxicity. The results of phase-2 studies in chronic heart failure patients showed that long-term oral treatment with propionyl-l-carnitine improves maximum exercise duration and maximum oxygen consumption over placebo and indicated a specific propionyl-l-carnitine effect on peripheral muscle metabolism. A multicenter trial on 537 patients showed that propionyl-l-carnitine improves exercise capacity in patients with heart failure, but preserved cardiac function.

This is the second report based on a survey of Divers Alert Network Asia-Pacific (DAN AP) members who dive with cardiovascular and respiratory conditions and diabetes. It examines the medical management of the divers' conditions, any diving modifications used to mitigate the risk and outcomes. An online cross-sectional survey was sent to 833 divers who had declared a targeted medical condition when applying for DAN AP membership between July 2009 and August 2013. Two-hundred-and-sixty-eight respondents (32%) provided sufficient information on their conditions to be included in the analyses. These included ischaemic heart disease (31), arrhythmias (20), cardiac septal defects (31), other cardiac conditions (10), hypertension (127), diabetes (25), asthma (40) and pneumothorax (5). Forty-nine per cent had sought specialist diving medical advice about their condition and 23% reported modifying their diving practices to mitigate their risk. The cohort had completed 183,069 career div...

Background. The mechanisms by which adrenaline may enhance defibrillation success rate, is poorly understood. Objectives. To study electrophysiological effects of adrenaline during short exposure to global ischemia. Methods. In isolated perfused feline hearts, coronary perfusion was eliminated repeatedly for 1 min with 10 min reperfusion intervals. Treatment included: (1) continuous perfusion alone—control, (2) global ischemia alone, (3) adrenaline (10−7 M) during perfusion, (4) adrenaline (10−7 M) during global ischemia (n = 10), in separate hearts, (5) control and higher adrenaline concentration (1 × 10−6 M), (6) during perfusion, (7) during global ischemia (n = 9). Measurements during pacing included: (1) diastolic threshold of excitability; (2) refractoriness; (3) epicardial conduction time; and (4) all tissue resistivity to indirectly detect changes in passive properties of conduction. Measurements during 1 min (or 90 sec) of electrically induced ventricular fibrillation included—all tissue resistivity and, based on maximal entropy spectral analysis and normalized entropy, rate of arrhythmia and degree of arrhythmia organization. Results. Adrenaline (10−7 M) during global ischemia vs control caused spontaneous arrhythmia termination, increased threshold significantly but reduced conduction time. Higher adrenaline concentration (1 × 10−6 M) during global ischemia improved the passive properties of conduction and arrhythmia organization and reduced arrhythmia rate. Global ischemia alone increased conduction time but had a deleterious effect on passive properties. Adrenaline (10−7 M) during perfusion improved conduction, but did so less than during global ischemia. Higher adrenaline concentration during perfusion (10−6 M) improved arrhythmia organization and caused spontaneous arrhythmia termination but again less than during global ischemia. Conclusions. During short periods of global ischemia adrenaline improved the passive properties of conduction and arrhythmia organization, reduced arrhythmia rate and increased its spontaneous termination. Such changes may be operative in improving defibrillation success.

Angina pectoris is the most prevalent symptomatic manifestation of ischemic heart disease, frequently leads to a poor quality of life, and is a major cause of medical resource consumption. Since the early descriptions of nitrite and nitrate in the 19(th) century, there has been considerable advancement in the pharmacologic management of angina. Areas covered: Management of chronic angina is often challenging for clinicians. Despite introduction of several pharmacological agents in last few decades, a significant proportion of patients continue to experience symptoms (i.e., refractory angina) with subsequent disability. For the purpose of this review, we searched PubMed and Cochrane databases from inception to August 2016 for the most clinically relevant publications that guide current practice in angina therapy and its development. In this article, we briefly review the pathophysiology of angina and mechanism-based classification of current therapy. This is followed by evidence-base...

THIS STUDY WAS TO ASSESS THE USEFULNESS OF THE CHANGES IN LEFT VENTRICULAR (LV)SYSTOLIC TIME INTERVALS AFTER PHENYLEPHRINE ADMINISTRATION FOR THE DETECTION OF HIGH RISK PATIENTS SOON AFTER ACUTE MYOCARDIAL INFARCTION BY CORRELATION WITH THE ANGIOGRAPHIC AND VENTRICULOGRAPHIC FINDINGS. THE PROCEDURE WAS PERFORMED IN 76 CONSECUTIVE PATIENTS (GROUP I) ON THE 4TH POST-INFARCTION DAY AND IN12 NORMAL SUBJECTS (GROUP II) FREE OF CORONARY ARTERY DISEASE. IN 20 PATIENTSWITH LV EJECTION FRACTION < = 40% (SUBGROUP IA) THE PRE-EJECTION PERIOD (PEP)/LV EJECTION TIME (ET) RATIO INCREASED FROM 0.416 +_ 0.107 TO 0.535 +- 0.102 (P = 0.01) AFTER PHENYLEPHRINE WHEREAS IN THE REMAINING 56 PATIENTS (SUBGROUP IB) WITH LV EJECTION FRACTION > 40% AND THE 12 NORMALS THE PEP/LVET INCREASED NON-SIGNIFICANTLY. OF PATIENTS WITH LV EJECTION FRACTION > 40% A SUBSET OF 20 PATIENTS WAS DISTINGUISHED WITH PROXIMAL STENOSIS IN BOTH LEFT ANTERIOR DESCENDING AND EITHER A DOMINANT RIGHT OR LEFT CIRCUMFLEX CORONARY ARTERY (SUBSET IB-A). IN THESE THE PEP/LVET INCREASED FROM 0.347 +- 0.056 TO 0.445 +- 0.019 (P= 0.0001) AFTER PHENYLEPHRINE; WHILE IN THE REMAINING 36 PATIENTS (SUBSET IB-B) WITHOUT PROXIMAL LESIONS IN 2 MAIN ARTERIES THE PEP /LVET INCREASED NON-SIGNIFICANTLY. IN CONCLUSION THE PEP/LVET RESPONSE TO PHENYLEPHRINE ADMINISTRATION EARLY AFTER ACUTE MYOCARDIAL INFARCTION IS A PRECISE, SAFE, NON-INVASIVE BEDSIDE METHOD FOR EARLY STRATIFICATION OF THESE PATIENTS.

Purpose: Myocardial infarct mediates an inflammatory response whose intensity limits the recovery of the damaged tissue and its function. In the present work, we evaluate the efficacy of immunomodulatory hIL10 gene hydrofection on acute myocardial infarct in pig. Methods: Pigs recently infarcted by right coronary artery block were injected with 50 ml saline solution containing the naked gene at 2 or 7 ml/s through coronary sinus. Blood samples were collected from coronary sinus before gene injection, 2 and 72 hours later for protein quantification. Heart tissue samples from normal and infarcted tissue were collected 72 hours post-transfection to evaluate the efficiency of gene delivery and decoding The results: hIL10 protein translation yielded more than 200 protein molecules/cell in normal tissue and was always higher than in infarcted areas. Coronary sinus plasma concentration of hIL10 protein reached 50 pg/ml as average. The histopathological evaluation of peri-infarct and infarct areas showed that interleukin 10 hydrofection mediated anti-inflammatory effects, as evidenced by reduced edema and cell infiltration. Conclusions: Heart hydrofection of hIL10 gene in infarct-induced pigs mediates local expression of cytokine in normal and infarcted tissue, resulting in reduced acute response triggered by the ischemic episode induced experimentally.

To evaluate whether hourly changes in fine particle (PM(2.5), diameter&lt;2.5 microm) exposure or outdoor particle concentrations are associated with rapid ischaemic responses. 41 non-smoking elderly people with coronary heart disease were followed up with biweekly clinic visits in Helsinki, Finland. The occurrence of ST segment depressions &gt;0.1 mV was recorded during submaximal exercise tests. Hourly variations in personal PM(2.5) exposure and outdoor levels of PM(2.5) and ultrafine particles (&lt;0.1 microm) were recorded for 24 h before a clinic visit. Associations between particulate air pollution and ST segment depressions were evaluated using logistic regression. Both personal and outdoor PM(2.5) concentrations, but not outdoor ultrafine particle counts, were associated with ST segment depressions. The odds ratio (per 10 microg/m(3)) for personal PM(2.5) concentration during the hour preceding a clinic visit was 3.26 (95% CI 1.07 to 9.99) and for 4 h average outdoor PM(2.5)...