Takotsubo cardiomyopathy triggered by status epilepticus: case report and literature review.

Takotsubo cardiomyopathy (TC) is acute stress-induced cardiomyopathy with characteristic transient wall motion abnormalities. TC has a clinical presentation similar to an acute coronary syndrome, including chest pain or dyspnoea, ECG changes and elevated cardiac enzymes. TC often occurs after emotional stress. There are approximately 50 TC cases reported related to seizure activity, and our review revealed 15 articles which were associated with status epilepticus. This condition can be a serious complication of seizures. We report a case of TC after status epilepticus in a patient who had been seizure-free for 20 years.

Late Strut Fracture Within a Partially Resorbed Bioresorbable Vascular Scaffold: A Possible Cause of Late Scaffold Thrombosis and Acute Coronary Syndrome.

The Bioresorbable Vascular Scaffold (BVS, Abbott Vascular, Santa Clara, Cal, USA) is an exciting advance in percutaneous coronary intervention providing a temporary drug eluting scaffold resorbed in two to five years. We present two cases of late scaffold thrombosis associated with strut fracture during the period of resorption, at 20 and 24 months following BVS implantation. We propose luminal migration of malapposed struts following strut fracture during resorption as a potential mechanism for late scaffold thrombosis and acute coronary syndrome.

Prevalence and outcomes of trans-radial access for percutaneous coronary intervention in contemporary practise.

BACKGROUND: Trans-radial access for percutaneous coronary intervention (PCI) has been associated with lower vascular complication rates and improved outcomes. We assessed the current uptake of trans-radial PCI in Victoria, Australia, and evaluated if patients were selected according to baseline bleeding risk in contemporary clinical practise, and compared selected clinical outcomes. METHODS: PCI data of all patients between 1st January 2013 and 31st December 2014 were analysed using The Victorian Cardiac Outcomes Registry (VCOR). Propensity-matched analysis was performed to compare the clinical outcomes. RESULTS: 11,711 procedures were analysed. The femoral route was the predominant access site (66%). Patients undergoing trans-radial access PCI were younger (63.9±11.6 vs. 67.2±11.8; p<0.001), had a higher BMI (28.9±5.5 vs. 28.5±5.2; p<0.001), more likely to be male (80.0 vs. 74.9%;p<0.001), less likely to have presented with cardiogenic shock (0.9 vs. 2.8%; p<0.001) or have the following comorbidities: diabetes (19.8 vs. 23.1%; p<0.001), peripheral vascular disease (2.9 vs. 4.3%; p=0.005) or renal impairment (13.6 vs. 22.1%; p<0.001). The radial group had less bleeding events (3.2 vs. 4.6%; p<0.001) and shorter hospital length of stay (3.1±4.7 vs. 3.3±3.9; p=0.006). There was no significant difference in mortality (1.0 vs. 1.4%; p=0.095). CONCLUSIONS: Trans-femoral approach remains the dominant access site for PCI in Victoria. The choice of route does not appear to be selected by consideration of bleeding risk. The radial route is associated with improved clinical outcomes of reduced bleeding and length of stay consistent with previous findings, and this supports the efficacy and safety of trans-radial PCI in real-world clinical practise.

Assessing the Value of BMI and Aerobic Capacity as Surrogate Markers for the Severity of Left Ventricular Diastolic Dysfunction in Patients with Type 2 Diabetes Who Are Obese.

Left ventricular diastolic dysfunction (LVDD) is one of the earliest signs for abnormal cardiac function in patients with type 2 diabetes (T2DM). It is important to explore the risk factors that will assist in identifying the severity of the LVDD in this population. We examined the influences of fitness and fatness on the level of left ventricular (LV) impairment in patients with T2DM. Twenty-five patients (age: 64.0 ± 2.5 years, body mass index [BMI] = 36.0 ± 1.5 kg/m(2), mean ± standard error of measurement) with T2DM and preserved systolic function, but impaired diastolic function, mitral valve (MV) E/e', participated in the study. LV function was assessed using a stress echocardiograph, aerobic power was assessed with a sign- and symptom-limited graded exercise test, and the fatness level was assessed using Dual-energy X-ray absorptiometry and BMI. Patients in the higher 50% of BMI had higher lateral and septal MV E/e' (∼34% and ∼25%, respectively, both P < 0.001), compared to those in the lower 50% of BMI, with no difference in LV ejection fraction (LVEF) (P > 0.05). In addition, a higher BMI correlated with a higher lateral (r = 0.62, P < 0.001) and septal (r = 0.56, P < 0.01) E/e'. There was no such relationship for VO2peak. BMI and VO2peak were not correlated with LV systolic function (ejection fraction). In individuals with T2DM and diastolic dysfunction, a higher BMI was associated with worsening diastolic function independent of their aerobic capacity. The data provide a simple and practical approach for clinicians to assist in the early identification and diagnostics of functional changes in the heart diastolic function in this population.

Muscle atrophy in patients with Type 2 Diabetes Mellitus: roles of inflammatory pathways, physical activity and exercise.

Muscle atrophy is caused by an imbalance in contractile protein synthesis and degradation which can be triggered by various conditions including Type 2 Diabetes Mellitus (T2DM). Reduced muscle quality in patients with T2DM adversely affects muscle function, the capacity to perform activities of daily living, quality of life and ultimately may increase the risk of premature mortality. Systemic inflammation initiated by obesity and prolonged overnutrition not only contributes to insulin resistance typical of T2DM, but also promotes muscle atrophy via decreased muscle protein synthesis and increased ubiquitin-proteasome, lysosomal-proteasome and caspase 3- mediated protein degradation. Emerging evidence suggests that the inflammation-sensitive Nuclear Factor κ B (NF-κB) and Signal Transducer and Activator of Transcription 3 (STAT3) pathways may contribute to muscle atrophy in T2DM. In contrast, exercise appears to be an effective tool in promoting muscle hypertrophy, in part due to its effect on systemic and local (skeletal muscle) inflammation. The current review discusses the role inflammation plays in muscle atrophy in T2DM and the role of exercise training in minimising the effect of inflammatory markers on skeletal muscle. We also report original data from a cohort of obese patients with T2DM compared to age-matched controls and demonstrate that patients with T2DM have 60% higher skeletal muscle expression of the atrophy transcription factor FoxO1. This review concludes that inflammatory pathways in muscle, in particular, NF-κB, potentially contribute to T2DM-mediated muscle atrophy. Further in-vivo and longitudinal human research is required to better understand the role of inflammation in T2DM-mediated atrophy and the anti-inflammatory effect of exercise training under these conditions.

Synchronous cardiac arrest in monozygotic twins with hypertrophic cardiomyopathy--is sudden cardiac death genetically pre-programmed?

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is a myocardial disorder characterised by left ventricular hypertrophy (LVH) in the absence of another cardiac or systemic disease capable of producing the magnitude of LVH evident. HCM causes variable symptoms and is one of the leading causes of sudden cardiac death (SCD) in young adults. While various phenotypic features of HCM among monozygotic twin pairs are not uncommonly reported, occurrence of synchronous cardiac arrest among them is not known from literature. CASE PRESENTATION: We present a case of monozygotic twins with HCM who both had a cardiac arrest post physical exertion in 63rd year of their lives. CONCLUSION: This case highlights potential genetics predisposition of cardiac arrest in patients with HCM despite having different phenotypic expression. SCD may be the only manifestation of patients with HCM. Decision of implantable cardioverter-defibrillator (ICD) placement for primary prevention of SCD should be based on the recommended guidelines, clinical judgment and patient's preference.

Clinical utility of exercise training in heart failure with reduced and preserved ejection fraction.

Reduced exercise tolerance is an independent predictor of hospital readmission and mortality in patients with heart failure (HF). Exercise training for HF patients is well established as an adjunct therapy, and there is sufficient evidence to support the favorable role of exercise training programs for HF patients over and above the optimal medical therapy. Some of the documented benefits include improved functional capacity, quality of life (QoL), fatigue, and dyspnea. Major trials to assess exercise training in HF have, however, focused on heart failure with reduced ejection fraction (HFREF). At least half of the patients presenting with HF have heart failure with preserved ejection fraction (HFPEF) and experience similar symptoms of exercise intolerance, dyspnea, and early fatigue, and similar mortality risk and rehospitalization rates. The role of exercise training in the management of HFPEF remains less clear. This article provides a brief overview of pathophysiology of reduced exercise tolerance in HFREF and heart failure with preserved ejection fraction (HFPEF), and summarizes the evidence and mechanisms by which exercise training can improve symptoms and HF. Clinical and practical aspects of exercise training prescription are also discussed.

Treatment of hypertension in heart failure with preserved ejection fraction.

Prevalence of Heart Failure with Preserved Ejection (HFPEF) has been rising steadily in the recent past. Studies have shown that at least half of patients presenting with symptoms and signs of heart failure (HF) have preserved left ventricular ejection fraction, i.e. HFPEF, and that this portion of the HF population consists predominantly of women, older age group, and people with hypertension and other cardiovascular risk factors. The morbidity and mortality associated with HFPEF are much higher than the normal population. Chronic hypertension is the most common cause in addition to age, with suggestion of up to 60% of patients with HFPEF being hypertensive. Addressing the specific aetiology and aggressive risk factor modification remain the mainstay in the treatment of HFPEF. Current guidelines recommend the management should involve treatment of hypertension, control of heart rate, venous pressure reduction, and prevention of myocardial ischemia. This review aims to discuss the role of hypertension in the pathophysiology, risk stratification and prognosis of HFPEF, as well as the current available data on various antihypertensive options in this population.

Heart failure with preserved ejection fraction - unwinding the diagnosis mystique.

A precise diagnosis of diastolic dysfunction is often difficult and requires invasive techniques to determine left ventricular volume, relaxation, and compliance properties. At this current point of time there is no single non-invasive index available to adequately reflect diastolic function, perhaps because of the numerous factors that can alter diastolic function. In most clinical settings, diastolic function is estimated using Doppler echocardiography. Cardiac magnetic resonance imaging (CMRI) is yet another emerging modality for diastolic function analysis. Here we present a comprehensive review of the various parameters used to assess diastolic function as part of diagnosis of clinical syndrome "Heart failure with preserved ejection fraction (HFPEF)".

Effects of intravenous caffeine on fractional flow reserve measurements in coronary artery disease.

BACKGROUND: Intravenous adenosine is used to minimise the coronary micro-resistance to achieve maximal hyperaemia along with nitrates for optimal fractional flow reserve (FFR) measurements. We hypothesise that caffeine, being a competitive inhibitor of adenosine, would influence adenosine-mediated FFR readings. METHODS: Consecutive patients undergoing angiogram and FFR measurements were enrolled after abstaining from caffeine for 24 h. Patients with any contraindications to intravenous adenosine or caffeine were excluded. FFR measurements were taken using nitrates and adenosine pre and post 4 mg/kg intravenous caffeine administration and results were compared. RESULTS: 10 patients were analysed (80% men, age 59.9±9.4, weight 87.5±15.6). Baseline caffeine levels were undetectable in all patients and increased significantly postintravenous caffeine administration (16.4±5.5 µg/mL). Baseline preadenosine FFR values were similar before and after caffeine administration (0.91±0.06 vs 0.91±0.07; p=0.41). Postadenosine FFR readings were 0.79±0.07, which increased non-significantly to 0.82±0.11 postcaffeine (p=0.15). Two significant FFR readings (≤0.8) changed to non-significant after caffeine administration (0.77-0.93 and 0.8-0.91). CONCLUSIONS: Caffeine may affect FFR results in some patients. Larger studies are warranted to clarify the extent and magnitude of caffeine/adenosine interaction particularly due to ubiquitous nature of caffeine and increasing importance of FFR in clinical practice.

Predictors and outcomes of early coronary angiography in patients with prior coronary artery bypass surgery presenting with non-ST elevation myocardial infarction.

INTRODUCTION: The best strategy in patients with prior coronary artery bypass graft surgery (CABG) who present with non-ST elevation myocardial infarction (NSTEMI) remains less well defined. We compare the characteristics, therapeutic interventions and outcomes of patients with prior CABG presenting with NSTEMI. METHODS: All patients who presented to our hospital during 2007-2012 with available electronic records were analysed retrospectively. Outcomes were compared between patients who underwent coronary angiography or percutaneous coronary intervention (PCI) versus those who were treated medically. RESULTS: A total of 117 patients were analysed. Of that, 79 patients were managed medically while 38 underwent early angiography, of which only 11 (9.5%) received PCI. Patients treated medically (did not undergo angiography) were older (74±10 vs70±8; p=0.05). ECG changes were the only independent predictor for early angiography (OR 0.4, 95% CI 0.15 to 0.99; p=0.05) while recurrent chest pain (OR 0.2, 95% CI 0.05 to 0.97; p=0.05) predicted PCI on multivariate analysis. The PCI group had higher Global Registry of Acute Cardiac Events (GRACE) score (176±29 vs 150±31; p=0.01). No significant difference was found in readmission rates, morbidity (unstable angina pectoris, NSTEMI, ST elevation myocardial infarction (STEMI), or combination) or mortality at 12 months between the groups who underwent angiography, PCI, or treated medically on univariate and multivariate analysis. CONCLUSIONS: The opportunity to intervene in prior CABG patients presenting with NSTEMI is often low. Initial medical management may be a reasonable option in carefully selected patients particularly in the absence of ongoing symptoms, ECG changes or very high GRACE scores. Further studies are required to evaluate the safety of non-invasive strategies in managing this population.

Use of ivabradine and atorvastatin in emergent orthopedic lower limb surgery and computed tomography coronary plaque imaging and novel biomarkers of cardiovascular stress and lipid metabolism for the study and prevention of perioperative myocardial infarction: study protocol for a randomized controlled trial.

BACKGROUND: The incidence of perioperative myocardial infarction (PMI) globally is known to be around 2 to 3% and can prolong hospitalization, increased morbidity and mortality. Little is known about the pathophysiology and risk factors for PMI. We investigate the presence of elevated novel cardiac markers and preoperative coronary artery plaque through contemporary laboratory techniques to determine the correlation with PMI, as well as studying ivabradine and atorvastatin as protective pharmacotherapies against PMI in the context of orthopedic surgery. METHODS/DESIGN: We aim to enroll 200 patients aged above 60 years who suffer from neck of femur fracture requiring surgery. Patients will be randomized to four arms (no study drugs, atorvastatin only, ivabradine only and ivabradine and atorvastatin). Our primary outcome is incidence of PMI. All patients will receive an electrocardiogram, cardiac echocardiography, measurement of novel cardiac biomarkers and computed tomography (CT) coronary angiography. A telephone interview post discharge will be conducted at 30 days, 60 days and 1 year. DISCUSSION: We postulate that ivabradine and atorvastatin will reduce the rate and magnitude of PMI following surgery by reducing heart rate and attenuating catecholamine-induced tachycardia postoperatively. Secondly, we postulate that postoperative reduction in heart rate and catecholamine-induced tachycardia with ivabradine will correlate with a reduction in cardiovascular novel biomarkers which will reduce atrial stretch and postoperative incidence of arrhythmia. We aim to demonstrate that treatment with ivabradine and atorvastatin will cause a reduction in the incidence and magnitude of PMI, the benefit of which is derived primarily in patients with greater atherosclerotic burden as measured by higher CT coronary calcium scores. TRIAL REGISTRATION: This study protocol has been listed in the Australia New Zealand Clinical Trial Registry (registration number: ACTRN12612000340831) on 23 March 2012.

Radiation exposure with the radial approach for diagnostic coronary angiography in a centre previously performing purely the femoral approach.

INTRODUCTION: Use of the radial approach for coronary angiography and percutaneous coronary intervention (PCI) is known to improve many patient outcome measures. However, there is some concern that it may be associated with increased patient radiation exposure. This study explores radiation exposure with the radial approach compared with the femoral approach in a centre previously performing purely femoral approach. PATIENTS AND METHODS: Data was collected retrospectively for all patients undergoing diagnostic coronary angiography over a six month period. PCIs and procedures with inherent technical difficulty or use of additional techniques (graft studies, optical coherence tomography, fractional flow reserve) were excluded. Dose area product (DAP) and fluoroscopy time (FT) were analysed for all remaining procedures (n=389), comparing radial (n=109) and femoral (n=280) approaches. RESULTS: The overall mean FT for transradial cases (7.45 mins) was significantly higher than for transfemoral cases (4.59 mins; p<0.001). The overall mean DAP for transradial cases (95.64 G Gycm(2)) was significantly higher than for transfemoral cases (70.25 Gycm(2), p<0.05)). Neither the FT nor the DAP decreased over the six month period. CONCLUSION: The radial approach was associated with significantly higher DAP and FT compared to the femoral approach during an initial introductory phase which was likely insufficient to develop radial proficiency. The results of this study are consistent with previous studies and may influence choice of access for non-emergent diagnostic coronary angiography before radial proficiency has been established, particularly for patients more susceptible to radiation risks.

Rivaroxaban in acute coronary syndromes--is it prime time?

Arterial thrombosis in acute coronary syndrome (ACS) is associated with activation of platelets and the coagulation cascade. Persistent thrombin levels have been reported after ACS in such patients. Novel oral anticoagulants without a need of close monitoring and frequent blood tests such as warfarin can provide a chronic beneficial effect on recurrent ischaemic events in such a population. Rivaroxaban, a new oral factor Xa inhibitor, has been tried for this indication in the 'Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects With Acute Coronary Syndrome ACS 2-Thrombolysis In Myocardial Infarction 51' (ATLAS ACS 2-TIMI 51) trial using a low dose regimen in an attempt to balance the adverse effects of bleeding related to chronic anticoagulation on background of dual antiplatelet therapy for ACS, and the beneficial effects on recurrent coronary ischemia. The role of rivaroxaban in this context has been discussed in detail in this review.

Platypnoea orthodeoxia after hepatic surgery.

Platypnoea orthodeoxia is a rare clinical syndrome characterised by dyspnoea and deoxygenation exhibited in upright position with improvement in supine posture. Previously described aetiologies include cardiac (pericardial effusion or constrictive pericarditis), pulmonary (pneumonectomy, emphysema or amiodarone toxicity), abdominal (cirrhosis or ileus) or vascular (abdominal aortic aneurysm) causes. We report an unusual case of platypnoea orthodeoxia associated with patent foramen ovale and partial hepatic resection.