Heart failure (HF) is a complex condition which has a mortality and high hospital readmission rate [ [1] Al-Omary M.S. Khan A.A. Davies A.J. Fletcher P.J. Mcivor D. Bastian B. Oldmeadow C. Sverdlov A.L. Attia J.R. Boyle A.J. Outcomes following heart failure hospitalization in a regional Australian setting between 2005 and 2014. ESC Heart Failure. 2018; 5 (http://doi.org/10.1002/ehf2.12239): 271-278 Crossref PubMed Scopus (0) Google Scholar ]. Despite the existence of evidence-based guidelines for HF, there remain gaps in the delivery of inpatient care.

Pericardial effusion is a rare complication of cancer; pericardiocentesis serves as both a diagnostic and therapeutic approach to patients with this presentation. We reviewed the aetiologies and outcomes of patients treated with pericardiocentesis in a major oncology centre.

A 29-year-old woman presented with abdominal pain, pyrexia, and diarrhoea. Her medical history included polycystic ovarian syndrome and Grave disease. Physical examination revealed tachycardia and diffuse abdominal tenderness. She was treated for gastroenteritis with intravenous fluids but continued to have profuse diarrhoea with ongoing abdominal pain. She was commenced on intravenous ceftriaxone and a contrast computed tomography abdomen was performed showing mild ileitis. On day 2 she experienced typical ischaemic chest pain with inferior ST segment elevation on electrocardiogram. She underwent a coronary angiogram, which found no obstructive coronary artery disease. Her troponin was 113,998 ng/L and stool cultures were positive for Salmonella typhimurium. A presumptive diagnosis of Salmonella myocarditis was made and confirmed with cardiac magnetic resonance imaging (MRI), which demonstrated delayed subepicardial gadolinium enhancement in the inferior wall. She completed 9 days of intravenous ceftriaxone prior to discharge. A repeat cardiac MRI at 3 months showed persisting abnormal enhancement and an endomyocardial biopsy revealed non–specific lymphocytic infiltrate, consistent with recovering myocarditis. Myocarditis is inflammation of the heart muscle and symptoms are usually non–specific. Studies suggest that myocarditis may account for 12–20% of sudden deaths in adults under the age of 40 [ [1] Feldman A.M. McNamara D. Myocarditis. N Engl J Med. 2000; 343: 1388-1398 Crossref PubMed Scopus (961) Google Scholar ]. Although uncommon, myocarditis is a recognised complication of Salmonella infection and is associated with high mortality [ [2] Burt C.R. Proudfoot J.C. Roberts M. Horowitz R.F. Fatal myocarditis secondary to Salmonella septicaemia in a young adult. J Emerg Med. 1990; 8: 295-297 Abstract Full Text PDF PubMed Scopus (22) Google Scholar ]. Bacterial myocarditis is rare in immunocompetent patients and only very occasional cases of Salmonella myocarditis have been reported. Cardiac MRI is one of the most comprehensive and accurate diagnostic tools for myocarditis [ [3] Friedrich M.G. Marcotte F. Cardiac magnetic resonance assessment of myocarditis. Circ Cardiovasc Imaging. 2013; 6: 833-839 Crossref PubMed Scopus (115) Google Scholar ]. To our knowledge, this is the first case report of Salmonella myocarditis confirmed using cardiac MRI.

Staphylococcus aureus is widely reported to be the most common bacterial cause of myocarditis, and usually occurs in the setting of bacteraemia and sepsis. Rarely, it occurs without associated infective endocarditis. Previous case reports of S. aureus myocarditis occur almost exclusively in immunocompromised patients. We report a case of S. aureus myocarditis with associated inflammatory thrombus in an immunocompromised patient. A 45-year-old man with a previous history of rheumatoid arthritis on long-term methotrexate presented with septic shock. He was found to have a methicillin-sensitive S. aureus bacteraemia. The patient subsequently developed olecranon bursitis requiring surgical wash out. Transthoracic echocardiogram revealed a very atypical echodense mass in the left ventricular apex, with normal systolic function and no associated valvular abnormalities. Cardiac magnetic resonance imaging showed oedema in the endomyocardium, consistent with acute myocarditis, associated with an apical mural thrombus. Repeat cardiac magnetic resonance 3 weeks following discharge from hospital showed marked improvement in endomyocardial oedema and complete resolution of the apical mural thrombus. He was treated with a 12-week course of antibiotics and anticoagulated with apixaban. Staphylococcal myocarditis without endocarditis is a rare disease entity, and significant disease manifestations can arise even without valvular involvement. Cardiac magnetic resonance is a useful diagnostic tool in bacterial myocarditis and characterisation of apical masses detected on transthoracic echocardiogram. The role of direct acting oral anticoagulants in this context remains unclear.

A 20-year-old man presented with palpitations, dyspnoea, and presyncopal symptoms after exercise. He was found to have a significantly elevated troponin. ECG met voltage criteria for left ventricular hypertrophy and no arrhythmia was detected on continuous ECG monitoring. A coronary angiogram showed no coronary artery disease. A transthoracic echocardiogram showed severe asymmetric septal hypertrophy without left ventricular outflow tract obstruction, and a moderately dilated left atrium. Exercise stress testing did not provoke any further arrhythmia or abnormal haemodynamic response to exercise. Cardiac magnetic resonance imaging (CMR) demonstrated asymmetric septal hypertrophy predominantly affecting the mid to apical septum with wall thickness up to 25mm and there was some apical aneurysmal dilatation and apical akinesis. There was late gadolinium enhancement (LGE) comprising up to 30% of the total myocardium. A diagnosis of hypertrophic cardiomyopathy (HCM) was made, and he was commenced on metoprolol and received an automatic implantable cardioverter-defibrillator (AICD) for primary prevention of sudden cardiac death (SCD) on the basis of young age at diagnosis and the extent of LGE. In the following months, he received an AICD shock and device interrogation revealed ventricular tachycardia.

Left ventricular diastolic dysfunction is a well-described complication of systemic hypertension. However, less is known regarding the effect of chronic pressure overload on right ventricular (RV) diastolic function. We hypothesized that pulmonary hypertension (PHT) is associated with abnormal RV early relaxation and that this would be best shown by invasive pressure measurement. Twenty-five patients undergoing right heart catheterization for investigation of breathlessness and/or suspected PHT were studied. In addition to standard measurements, RV pressure was sampled with a high-fidelity micromanometer, and RV pressure/time curves were analyzed. Patients were divided into a PHT group and a non-PHT group on the basis of a derived mean pulmonary artery systolic pressure of 25 mmHg. Eleven patients were classified to the PHT group. This group had significantly higher RV minimum diastolic pressure (5.1 +/- 6.6 vs. -0.1 +/- 3.3 mmHg, P = 0.03) and RV end-diastolic pressure (RVEDP; 11.0 +/- 6.3 vs. 3.8 +/- 3.7 mmHg, P = 0.004), and RV tau was significantly prolonged (53 +/- 32 vs. 31 +/- 13 ms, P = 0.04). There were strong correlations between RV t and RV minimum diastolic pressure (r = 0.93, P < 0.0001) and between RV t and RVEDP (r = 0.87, P < 0.0001). There was a trend toward increased RV contractility (end-systolic elastance) in the PHT group (0.73 +/- 0.21 vs. 0.52 +/- 0.21 mmHg/mL, P = 0.07) and a correlation between RV systolic pressure and first derivative of maximum pressure change (r = 0.58, P = 0.003). Stroke volumes were similar. Invasive measures of RV early relaxation are abnormal in patients with PHT, whereas measured contractility is static or increasing, which suggests that diastolic dysfunction may precede systolic dysfunction. Furthermore, there is a strong association between measures of RV relaxation and RV filling pressures.

R A L A B ST R A C T S Conclusion: Adult patients with ASD have an increased mortality compared to healthy controls. The risk does not change with age at operation. Those without closure of an ASD have a significantly higher mortality compared to those with closure. Even adult patients with ASDs that are considered hemodynamically un-important seem to carry an increasedmortality risk. Disclosure of Interest: None Declared

Purpose: The effect of chronic pressure overload on right ventricular (RV) diastolic function is unknown. We examined invasive measures of RV diastolic function in patients with a range of pulmonary pressures. Methods: Twenty-five patients (seven male, mean age 57.6) underwent right heart catheterisation for investigation of dyspnoea and/or suspected pulmonary hypertension (PH). These included nine patients with left ventricular diastolic dysfunction (LVDD), seven patients with scleroderma, two patients with scleroderma and LVDD, one patient with IPAH, one patient with severe mitral stenosis, one patient with interstitial lung disease and four ostensibly healthy subjects. RV pressure was sampled by a Radi PressureWire. RV systolic pressure (RVSP), RV minimum diastolic pressure (RVDP), RV dP/dt max and RV dP/dt min were obtained. RV end diastolic pressure (RVEDP) was defined as the pressure at 10% RV dP/dt max. RV isovolumic relaxation time (IVRT) was defined as the time between RV dP/dt min and the time at RVEDP during initial pressure decay. RV tau was determined using the method of Weiss. Patients were divided into a PH group (mPAP > 25 mmHg) and a non-PH group. Results: Eleven patients had mPAP > 25 mmHg. This group had higher RVSP, RVDP, RVEDP and longer RV tau. There was a trend to a longer IVRT. RV dP/dt min was greater in the PH group, reflecting the after load dependence of this measure. In contrast, RV dP/dt max (a surrogate of contractility) was similar.Tabled 1RVSP (mmHg)RVDP (mmHg)RV EDP (mmHg)dP/dt min (mmHg/s)dP/dt max (mmHg/s)RV tau (ms)IVRT (ms)PH56.0 ± 21.55.1 ± 6.611.0 ± 6.3−530 ± 219521 ± 20953 ± 3252 ± 25Non−PH30.0 ± 5.2−0.1 ± 3.33.8 ± 3.7−304 ± 78436 ± 14631 ± 1338 ± 16p0.0020.030.0040.0060.270.040.13 Open table in a new tab Conclusion: Pulmonary hypertension is associated with abnormal measures of RV active relaxation and increased RVEDP.

Introduction: PIMR is a novel index of pulmonary microvascular function calculated from PressureWire-derived distal pressure and flow. While PIMR has been reported in a large animal model of pulmonary arterial hypertension (PAH), its utility in the clinical setting has not been explored. Methods: Patients referred for diagnostic right heart catheterisation underwent Swan Ganz catheter and PressureWire (placed in 3rd order PA branch) measurement of pulmonary haemodynamics both before and during adenosine infusion. PIMR was calculated as mean transit time × (distal PA pressure − PA wedge pressure). Results: Thirty-eight subjects (average age 61 years) were studied including five normal, eleven PAH, fifteen heart failure with normal ejection fraction (HFNEF), five mitral valve disease, and two interstitial lung disease patients. Adenosine infusion resulted in 28% fall in pulmonary vascular resistance (PVR) and a 29% fall in systemic vascular resistance driven mainly by an increase in cardiac output (5.9 ± 0.3 L/min vs. 8.6 ± 0.4 L/min, p < 0.001). PIMR was closely related to PVR during adenosine (r = 0.63, p < 0.001). PIMR was higher in patients with transpulmonary gradient greater than 12 (6.9 ± 1.3 vs. 3.6 ± 0.9, p < 0.018) and in patients with PAH compared to those with HFNEF (10.5 ± 1.7 vs. 3.2 ± 0.4, p < 0.001). Conclusions: PIMR is closely related to PVR, suggesting that resistance in the pulmonary circulation occurs mainly at the microvascular level. While adenosine is an effective pulmonary vasodilator, its substantial effect on systemic resistance may make alternative agents such as PDE-5 inhibitors more attractive for pulmonary vasodilator challenge.

Purpose: Pulmonary wave reflection (PWV) is an important component of pulsatile hydraulic load on the right ventricle (RV). Pulmonary augmentation index (PAI) and time to inflection point (Ti) represent two indices of PWV. We observed the relationship between these indices and measures of static RV afterload in patients with a range of pulmonary pressures. Methods: Twenty patients (six male, mean age 58.6) underwent right heart catheterisation for the investigation of dyspnoea and/or suspected pulmonary hypertension. These included 10 patients with scleroderma, six patients with left ventricular diastolic dysfunction, one patient with interstitial lung disease, one patient with severe mitral stenosis and two ostensibly healthy subjects. In addition to standard measurements of pulmonary vascular resistance (PVR), mean pulmonary artery pressure (mPAP) and trans-pulmonary gradient (TPG), pulmonary artery pressure was measured by a Radi PressureWire. PAI was calculated as the ratio of pulmonary artery systolic pressure minus the pressure at the inflection point of wave reflection over the pulmonary pulse pressure. Ti was defined as the time between the pulmonary artery diastolic pressure and the inflection point. Results: Mean TPG was 15 ± 10.6 mmHg, mean PVR was 2.8 ± 2.3 mmHg·min/l and mean mPAP was 29.5 ± 14.4 mmHg. There were significant positive correlations between the pulmonary augmentation index and TPG (r = 0.61, p < 0.005), mPAP (r = 0.50, p < 0.05) and PVR (r = 0.45, p < 0.05). There were significant inverse correlations between the time to inflection point and TPG (r = −0.60, p = 0.005), PVR (r = −0.57, p < 0.05) and a trend to an inverse correlation with mPAP (r = −0.43, p = 0.06). Conclusion: Increasing RV afterload is associated with changes in PWV.

OBJECTIVE:We aimed to identify the baseline prevalence of cardiac dysfunction in patients commencing clozapine, assess adherence with echocardiographic monitoring recommendations, and evaluate the utility and cost of echocardiographic monitoring for the development of clozapine-associated myocarditis and cardiomyopathy.METHODS:A retrospective longitudinal cohort study was undertaken of 159 consecutive patients from a major tertiary centre commencing clozapine in the period January 2002 to July 2009.RESULTS:Some 73% of patients had a baseline study, and 11% had a six-month follow-up study. Nine patients had abnormal left ventricular function at baseline. Myocarditis was identified in three patients, with all cases occurring within the first month of treatment and suspected on clinical grounds before an echocardiogram was performed. One case of possible cardiomyopathy was identified. The cost of echocardiographic screening in the first year of treatment was estimated at $AUD 209,356 per case of cardiomyopathy detected.CONCLUSION:The prevalence of cardiac dysfunction in patients commencing clozapine is high, and there are challenges in adhering with the recommended protocol for monitoring. Routine echocardiography is not useful in the detection of clozapine-associated myocarditis. Although cardiomyopathy may be identified, it is rare and associated with significant cost. Recommendations for routine echocardiographic monitoring should be re-examined.

Purpose: Diastolic dysfunction of the right ventricle (RV) in patients with scleroderma (Scl) may be associated with stress-induced pulmonary hypertension (PH). We hypothesised that resting measures of RV diastolic function may correlate with Dobutamine-induced changes in pulmonary artery systolic pressure (PASP) or pulmonary vascular resistance (PVR). The effect of Dobutamine on echocardiographic parameters of RV diastolic function is unknown. Methods: Twenty-four patients with Scl, nine patients with Scl and PH (PASP > 35 mmHg) and six controls underwent Dobutamine stress echocardiography. Peak systolic (S′), early (E′) and late (A′) diastolic velocities were measured from tissue Doppler images of the lateral tricuspid annulus. PASP and PVR were derived non-invasively. Results: There were no significant differences between the groups at baseline or at any level of Dobutamine with respect to E′, A′ or E′/A′ ratio. Overall, Dobutamine was associated with a biphasic response in E′ and A′ and a decrease in E′/A′. There was no correlation between baseline E′, A′ or E′/A′ with PASP, PVR or ΔPASP, ΔPVR at any level of Dobutamine in any group.Tabled 1ParameterDobutamine infusion rate (mcg/kg/min)pBaseline2.557.510S′ (cm/s)10.0311.9113.4914.2914.36<0.0001E′ (cm/s)8.539.159.258.817.710.0004A′ (cm/s)10.4911.2312.2513.1912.86<0.0001E′/A′0.860.870.790.690.61<0.0001 Open table in a new tab Conclusion: Dobutamine-induced stress was associated with a decrease in lateral tricuspid annular E′/A′ independent of Scl or Scl with PH. Baseline RV diastolic parameters were not correlated with Dobutamine-induced changes in pulmonary haemodynamics.

Purpose: Pulmonary hypertension (PH) is associated with a poor prognosis regardless of aetiology. Reduced pulmonary vascular capacitance, in addition to increased resistance, may be an important determinant of pulmonary afterload and thus increasing pulmonary pressure. Methods: Subjects referred for diagnostic right heart catheterisation with suspected PH underwent assessment of pulmonary haemodynamics pre- and post-IV adenosine using a pressure and temperature-sensing guidewire (PressureWire) positioned in a second order branch pulmonary artery (PA) providing high fidelity pressure measurement and thermodilution derived mean transit time (Tmn). Capacitance index (CI, mL/mmHg) was defined as 1000/(heart rate × PA pulse pressure × Tmn). Diastolic dysfunction (DD) was defined as LVEDP greater than 18 mmHg and PH as mean PA pressure greater than 25 mmHg. Results: Thirty-one consecutive patients were analysed: 10 with pulmonary arterial hypertension (PAH, either primary or secondary to scleroderma), six had DD with PH, seven had both scleroderma and DD, four had mitral valve disease and four were normal. Adenosine infusion resulted in decreased Tmn (0.47 ± 0.05 vs 0.33 ± 0.03, p < 0.001) and increased CI (1.79 ± 0.28 vs 2.33 ± 0.3, p < 0.005), but no change in heart rate nor mean PA pressure. Higher PA pressure was associated with lower CI, both pre adenosine (r = −0.62, p < 0.003) and post adenosine (r = −0.54, p < 0.003). Conclusion: Capacitance index is reduced with increasing severity of PH and to a greater extent in patients with PAH than those with DD. This novel index may have utility in early diagnosis and tracking subtle changes in haemodynamics in patients with PH.

Purpose: The effect of chronic pressure overload on the diastolic function of the right ventricle (RV) has not been well studied in humans. We explored the relationship between invasive measures of RV diastolic function and RV pressure across a range of patients with and without pulmonary hypertension. Methods: Eighteen patients undergoing diagnostic right heart catheterisation were studied. Six patients had left ventricular diastolic dysfunction (LVDD), six had scleroderma, two had LVDD and scleroderma, two had idiopathic pulmonary arterial hypertension and two patients were found to be normal after investigation. RV pressure was measured invasively by a Radi PressureWire sampling at 100 Hz. Afterload was measured by peak RV systolic pressure (RVSP). Diastolic function parameters of minimum RV diastolic pressure (minRVDP) and RV (dP/dt)min and RV end diastolic pressure (RVEDP) were derived. RV tau was calculated using the method of Weiss. All measurements were averaged over five cardiac cycles. Results:Tabled 1Parameter (range)RVSP (18.4–69.3 mmHg)minRVDP (−5.9 to 10.2 mmHg)RVEDP (−2.5 to 15.2 mmHg)RV tau (9–80 ms)r = 0.32p = nsr = 0.91p < 0.0001r = 0.94p < 0.0001RV (dP/dt)min (−200 to −856 mmHg/s)r = −0.89p < 0.0001r = −0.15p = nsr = −0.12p = ns Open table in a new tab RV tau was strongly associated with minRVDP and RVEDP but not with RVSP. RV (dP/dt)min was strongly correlated with RVSP but not minRVDP or RVEDP. Conclusion: RV tau is an afterload independent measure of RV relaxation, while RV (dP/dt)min is strongly inversely associated with peak RV systolic pressure. Early RV relaxation as measured by RV tau is an important determinant of RVEDP as well as minimum RV diastolic pressure.

Introduction: Functional assessment of the pulmonary vasculature is an important tool in the diagnosis of pulmonary hypertension. The effect of adenosine on pulmonary haemodynamics in left heart disease is not well understood Methods: Right heart catheterisation was performed in eight subjects with mean PA pressure (mPAP) >25 mm Hg. In four subjects this was due to scleroderma (SCL) whilst four patients had heart failure with normal ejection fraction (HFNEF) defined by a pulmonary capillary wedge pressure (PCWP, mm Hg) >18 mm Hg and an ejection fraction >50%. Invasive haemodynamic measures were obtained before and during an adenosine infusion (140 mcg/kg/mins) Results: Four SCL patients had a mean age of 58 ± 13 years, all were female and none were on pulmonary vasodilator therapy. Four HFNEF patients had a mean age of 62 ± 8 years, all were female and were receiving systemic antihypertensive therapy. The four patients with HFNEF all had LV end diastolic pressure >18 mm Hg (mean 21.5 ± 4.2 mm Hg). The effect of adenosine on pulmonary haemodynamics is summarised in the table: in patients with SCL, adenosine infusion resulted in a significant decrease in PVR in both groups, and an increase in CO in HFNEF patients. Despite the reduction in PVR, there was a trend to increased mPAP in HFNEF patients Conclusions: Adenosine is an effective pulmonary vasodilator. Further study is required to elucidate whether the effect on pulmonary arterial and wedge pressures may vary with the etiology of pulmonary hypertension.Tabled 1SCL preSCL adenosineHFNEF preHFNEF adenosinemPAP47.5 ± 12.945.3 ± 10.227.8 ± 5.930.3 ± 3.7PCWP15.3 ± 6.616.8 ± 6.618.2 ± 6.220.0 ± 5.0CO5.9 ± 1.78.1 ± 4.46.2 ± 1.510.1 ± 2.3†p<0.01 for paired t-test comparison with pre adenosine.PVR5.8 ± 2.34.2 ± 2.3†p<0.01 for paired t-test comparison with pre adenosine.1.6 ± 0.61.1 ± 0.4*p<0.05 for paired t-test comparison with pre adenosine.* p < 0.05 for paired t-test comparison with pre adenosine.† p < 0.01 for paired t-test comparison with pre adenosine. Open table in a new tab

Background: Transthoracic echocardiography (TTE) is a simple and low risk modality for defining cardiac structure and function. However the relative ease of use creates the potential for overuse in patients who may not obtain benefit, with subsequent cost considerations and increased burden on echocardiography services. In light of this, appropriateness criteria for the rational use of transthoracic echocardiography were developed and reported by the American College of Cardiology in 2007. We compared these criteria to local referral patterns for TTE at a metropolitan tertiary referral hospital.