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 AE 6:6 vs. À0:1AE 3:3 mmHg, P ¼ 0:03) and RV end-diastolic pressure (RVEDP; 11:0 AE 6:3 vs. 3:8 AE 3:7 mmHg, P ¼ 0:004), and RV τ was significantly prolonged (53 AE 32 vs. 31 AE 13 ms, P ¼ 0:04). There were strong correlations between RV τ and RV minimum diastolic pressure (r ¼ 0:93, P < 0:0001) and between RV τ and RVEDP (r ¼ 0:87, P < 0:0001). There was a trend toward increased RV contractility (end-systolic elastance) in the PHT group (0:73 AE 0:21 vs. 0:52 AE 0:21 mmHg/mL, P ¼ 0:07) and a correlation between RV systolic pressure and first derivative of maximum pressure change (r ¼ 0:58, P ¼ 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.Keywords: right ventricle, right ventricular function, diastolic function, pulmonary hypertension, heart failure. Systemic hypertension is recognized to be one of the major causes of diastolic dysfunction in the left ventricle.1 The hypertrophied myocardium becomes stiff, and abnormalities in both active myocardial relaxation and passive elastance are observed, eventually leading to an increase in left ventricular filling pressures and left atrial pressure. 2,3Evidence for a similar phenomenon occurring in the right ventricle (RV) has been sparse. Although it is a thinner-walled structure that is exposed to much lower absolute afterload, the law of Laplace dictates that the RV is subjected to increased wall stress under conditions of pulmonary hypertension (PHT). 4 Compensatory RV hypertrophy is often seen. 5 A recent study involving humans also demonstrated RV hypertrophy and collagen deposition, increased sarcomeric stiffness, and reduced titin phosphorylation in patients with pulmonary arterial hypertension compared with controls. 6In 1967, Burstin first described the association between PHT and the postsystolic isovolumic period in the RV, suggesting the presence of diast...
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.
A clinical decision rule using simple clinical variables has the potential to improve the yield of SPE/UPE. This rule however needs to be verified prospectively.
Staphylococcus aureus myocarditis is a rare diagnosis with a high mortality rate, usually seen in people who are immunocompromised. Here, we report a case of a 44-year-old man on methotrexate for rheumatoid arthritis who presented in septic shock and was diagnosed with staphylococcus aureus myocarditis. The myocarditis was associated with a left ventricular apical thrombus, with normal systolic function. The myocarditis and associated thrombus were characterised on transthoracic echocardiogram and subsequently on cardiac magnetic resonance imaging. Cardiac magnetic resonance (CMR) imaging showed oedema in the endomyocardium, consistent with acute myocarditis, associated with an apical mural thrombus. Repeat CMR 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. The patient was successfully managed with intravenous antibiotics and anticoagulation with complete recovery.
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