Outcomes of transcatheter aortic valve implantation in high surgical risk and inoperable patients with aortic stenosis: a single Australian Centre experience.

BACKGROUND: Degenerative aortic stenosis is the most common valvular heart disease in the elderly, and many patients are not suitable for aortic valve replacement surgery. Transcatheter aortic valve implantation (TAVI) is a new therapeutic option for selected patients at high risk for surgery. AIM: To evaluate the safety and efficacy of TAVI in Australian patients. METHODS: This is a prospective study of patients undergoing TAVI for severe symptomatic aortic stenosis at The Prince Charles Hospital, Brisbane, Australia between August 2008 and July 2013. Patients were at high risk of surgical aortic valve replacement, or inoperable, as deemed by a multidisciplinary 'heart team'. Outcomes include procedural success and complications, 30-day and 1-year mortality and stroke, combined end-points as outlined by the Valve Academic Research Consortium 2 consensus document. RESULTS: Two hundred and nine patients underwent TAVI during the study period. The mean age was 83.7 ± 6.7 years, and 101 (48%) were men. The valve systems utilised were as follows: Edwards-SAPIEN valve in 104 (49.5%), Medtronic CoreValve in 86 (41.2%) and Boston Scientific Lotus valve in 19 (9.3%) patients. Thirty-day and 1-year mortality rates were 5.7% and 11.5% respectively. Thirty-day and 1-year stroke rates were 4.3% and 6.2% respectively. The composite end-points of device success, early safety and clinical efficacy occurred in 80.4%, 27.3% and 68.4%. CONCLUSIONS: TAVI with various valve systems, delivered through several approaches, is feasible in high surgical risk and inoperable patients with severe aortic stenosis, with acceptable outcomes at short-term and intermediate-term follow up.

Percutaneous ASD closure in a large Australian series: short- and long-term outcomes.

AIM: To assess the clinical and echocardiographic outcomes in patients referred for device closure of atrial septal defects in a tertiary referral hospital in Australia. METHODS: A prospective follow-up study was performed on all patients who had device closure of a secundum atrial septal defect (ASD) from June 1999 to December 2007. Clinical and echocardiographic data at the time of implantation and follow-up is presented. RESULTS: 176 patients were referred for shunt closure of ASD. All patients had a significant shunt defined as a shunt with right heart dilatation and/or a shunt ratio of at least 1.5:1. The majority were female (67%) and the average age was 36.5 ± 22.7 years; age range 3-84. The average hospital admission time was 2.5 ± 1.7 days. The average follow-up occurred at 3.7 ± 3.6 months for the first follow-up and 26.3 ± 18.2 months (range 3 months-7.8 years) for the long-term follow-up. Baseline echocardiogram findings showed the majority had a normal left ventricular ejection fraction (99%); average LVEF=63.2 ± 7.2% while the right ventricle was dilated in 61% of patients. Procedure information: The average procedure time was 94.8 ± 36.4 min. Procedural imaging was performed using Transoesophageal echocardiography (TOE) in 107 cases (61%); Intracardiac Echocardiography (ICE) in 69 (39%). Device use was as follows: Amplatzer=156 cases, Helex=18, and Starflex=2. Postprocedure shunt assessment by transthoracic echocardiography showed successful closure (no shunt or trivial shunt) in 99% cases. Two patients were referred for inpatient surgery due to a significant residual shunt in one case and an unstable device in another. One patient who had an unstable device had their device repositioned successfully. Atrial arrhythmia was the most common complication occurring in the peri-implantation period in 12 cases (6%) with four further cases at final up. The high prevalence of right ventricular dilatation in 65% patients at baseline had improved significantly at the first and long term follow-up to 2% (p=0.0001). CONCLUSION: Device closure of secundum atrial septal defects in this large Australian cohort demonstrates a high procedural success rate with a low incidence of complications in the short and long term.

High-dose tirofiban with enoxaparin and inflammatory markers in high-risk percutaneous intervention.

AIM: The study assessed the benefit of high bolus dose tirofiban (HD-tirofiban) with enoxaparin compared with HD-tirofiban with unfractionated heparin (UFH). The study examined markers of platelet activation, thrombin generation and inflammation. MATERIALS AND METHODS: The study is a prospective single centre open-label trial of patients with high-risk acute coronary syndrome treated with percutaneous intervention (PCI) who were randomized to anticoagulation with UFH or enoxaparin with HD-tirofiban (25 microg kg(-1) bolus). This study measured a panel of platelet activation markers, inflammatory biomarkers and thrombus generation between the two groups. RESULT: Sixty patients undergoing high-risk PCI were enroled in the study. Platelet inhibition as assessed by whole blood aggregometry following HD-tirofiban infusion was similar in both the UFH and enoxaparin groups. CD40 ligand expression on platelets was significantly reduced following PCI with HD-tirofiban and either UFH or enoxaparin. Following PCI, there were significant reductions measured in other markers of platelet activation including PAC-1, P selectin, factor V/Va, platelet-monocyte aggregates and monocyte expression of Mac-1 as determined by analysis of venous blood samples using flow cytometry. Prothrombin fragment 1+2, D-dimer, von Willebrand factor and high sensitive C-reactive protein levels were significantly less post PCI in the enoxaparin group compared with those patients receiving UFH. CONCLUSION: The combination of HD tirofiban with enoxaparin resulted in an attenuated inflammatory response when compared with that of the combination of HD tirofiban with UFH.

Early invasive versus conservative strategies for unstable angina & non-ST-elevation myocardial infarction in the stent era.

BACKGROUND: In patients with unstable angina and non-ST-elevation myocardial infarction (UA/NSTEMI) two strategies are possible: a routine invasive strategy where all patients undergo coronary angiography shortly after admission and, if indicated, coronary revascularization; or a conservative strategy where medical therapy alone is used initially with selection of patients for angiography based on clinical symptoms or investigational evidence of persistent myocardial ischemia. OBJECTIVES: To determine the benefits of an invasive compared to a conservative strategy for treating UA/NSTEMI in the stent era. SEARCH STRATEGY: The Cochrane Central Register of Controlled Trials (Issue 3 2005), MEDLINE and EMBASE were searched from 1996 to September 2005 with no language restrictions. SELECTION CRITERIA: Included studies were prospective trials comparing invasive with conservative strategies in UA/NSTEMI. DATA COLLECTION AND ANALYSIS: We identified 5 studies (7818 participants). Using intention-to-treat analysis with random effects models, summary estimates of relative risk (95% confidence interval [CI]) were determined for primary end-points of all-cause death, fatal and non-fatal myocardial infarction; all-cause death or non-fatal myocardial infarction; and refractory angina. Further analysis of included studies was undertaken based on whether glycoprotein IIb/IIIa receptor antagonists were used routinely. Heterogeneity was assessed using chi-square and variance (I(2)) methods. MAIN RESULTS: In the all-study analysis, mortality during initial hospitalization showed a trend to hazard with an invasive strategy; relative risk 1.59 (95% CI 0.96 to 2.64). Mortality and myocardial infarction assessed at 2-5 years in two trials were significantly decreased by an invasive strategy with relative risk of 0.75 (95% CI 0.62 to 0.92) and 0.75 (95% CI 0.61 to 0.91) respectively. The composite end-point of death or non-fatal myocardial infarction was significantly decreased by an invasive strategy at several time points after initial hospitalization. The incidence of early (<4 months) and intermediate (6-12 months) refractory angina were both significantly decreased by an invasive strategy; relative risk 0.47 (95% CI 0.32 to 0.68) and 0.67 (95% CI 0.55 to 0.83) respectively, as were early and intermediate rehospitalization rates with relative risk 0.60 (95% CI 0.41 to 0.88) and 0.67 (95% CI 0.61 to 0.74) respectively. The invasive strategy was associated with a two-fold increase in the relative risk of peri-procedural myocardial infarction (as variably defined) and a 1.7-fold increase in the relative risk of bleeding. AUTHORS' CONCLUSIONS: An early invasive strategy is preferable to a conservative strategy in the treatment of UA/NSTEMI.

Differentiation of restrictive cardiomyopathy from pericardial constriction: assessment of diastolic function by radionuclide angiography.

Diastolic filling variables were studied in 12 patients with the hemodynamic features of constriction, of whom 5 had restrictive cardiomyopathy, 5 had pericardial constriction and 2 had combined pericardial constriction and restrictive cardiomyopathy. The values were compared with those in 10 normal subjects of comparable age. The filling fractions between 10% and 70% of the diastolic time interval were greater in patients with pericardial constriction than in those with restrictive cardiomyopathy (p less than 0.01 between 20% and 50%, p less than 0.05 at 10%, 60% and 70%), with no overlap. The filling fractions in patients with pericardial constriction were also greater than those in normal subjects between 10% and 60% of the diastolic time interval. The filling fraction was lower in patients with restrictive cardiomyopathy than in normal subjects at 40% of the diastolic time interval (p less than 0.05). The time to peak filling rate in patients with pericardial constriction was shorter (110 +/- 14 ms) than in those with restrictive cardiomyopathy (195 +/- 45 ms, p less than 0.01) or in normal subjects (173 +/- 32 ms, p less than 0.01). The percent of atrial contribution to left ventricular filling was higher in those with restrictive cardiomyopathy (45 +/- 17%) than in those with pericardial constriction (21 +/- 6%, p less than 0.05) or in normal subjects (24 +/- 9%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Inotropic effect of nicardipine in patients with heart failure: assessment by left ventricular end-systolic pressure-volume analysis.

Nicardipine, a new dihydropyridine calcium channel blocker, has been investigated for the treatment of coronary artery disease and heart failure. To assess the inotropic effect of nicardipine in humans independent of its vasodilator effect, equihypotensive doses of intravenous nitroprusside (mean infusion rate 65 +/- 13 micrograms/min) and nicardipine (mean dose 5.2 +/- 0.4 mg) were administered to 15 patients with heart failure (New York Heart Association functional classes II to IV, radionuclide left ventricular ejection fraction 0.15 +/- 0.02). Left ventricular micromanometer pressure and simultaneous radionuclide left ventricular volume were obtained at baseline, during nitroprusside infusion, during a second baseline period and during nicardipine infusion. Heart rate did not change significantly with either nitroprusside or nicardipine. Mean systemic arterial pressure decreased by an average of 21 mm Hg with both drugs. A greater decrease in left ventricular end-diastolic pressure occurred with nitroprusside (27 +/- 2 to 14 +/- 2 mm Hg, p less than 0.01) than with nicardipine (27 +/- 2 to 23 +/- 3 mm Hg, p less than 0.05), and pulmonary capillary wedge pressure decreased significantly only with nitroprusside. Cardiac index increased from 1.8 +/- 0.1 to 2.1 +/- 0.1 liters/min per m2 (p less than 0.05) with nitroprusside and to a greater extent from 1.7 +/- 0.1 to 2.4 +/- 0.1 liters/min per m2 (p less than 0.01) with nicardipine. Left ventricular ejection fraction increased with nicardipine (0.15 +/- 0.01 to 0.19 +/- 0.01, p less than 0.01), but not with nitroprusside. Peak positive first derivative of left ventricular pressure (dP/dt) decreased by 9% with both agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Lack of effect of coenzyme Q on left ventricular function in patients with congestive heart failure.

OBJECTIVES: This study evaluated the effects of oral therapy with coenzyme Q on echocardiographic and hemodynamic indexes of left ventricular function and on quality of life in patients with chronic left ventricular dysfunction. BACKGROUND: Coenzyme Q is a coenzyme for oxidative phosphorylation and an antioxidant and free radical scavenger. It has been claimed to improve symptoms, quality of life, left ventricular ejection fraction and prognosis in patients with cardiac failure. METHODS: Thirty patients with ischemic or idiopathic dilated cardiomyopathy and chronic left ventricular dysfunction (ejection fraction 26 +/- 6%) were randomized to a double-blind crossover trial of oral coenzyme Q versus placebo, each for 3 months. Right heart pressures, cardiac output and echocardiographic left ventricular volumes were measured at baseline and after each treatment phase, and quality of life was assessed using the Minnesota "Living With Heart Failure" questionnaire. It was calculated that to demonstrate an increase in left ventricular ejection fraction from 25% to 30% with a standard deviation of 5% using 95% confidence intervals with a power of 80% we would require 17 patients. RESULTS: Twenty-seven completed both treatment phases. There was no significant difference in left ventricular ejection fraction, cardiac volumes or hemodynamic and quality of life indices after treatment with coenzyme Q or placebo, although plasma coenzyme Q levels increased from 903 +/- 345 nmol/l(-1) to 2,029 +/- 856 nmol/l(-1). CONCLUSIONS: In patients with left ventricular dysfunction, treatment for three months with oral coenzyme Q failed to improve resting left ventricular systolic function or quality of life despite an increase in plasma levels of coenzyme Q to more than twice basal values.

Effects of atrial natriuretic peptide on myocardial contractile and diastolic function in patients with heart failure.

Atrial natriuretic peptide alters left ventricular performance in patients with heart failure. To assess the direct effects of this hormone on myocardial function, its actions were compared with those of the pure vasodilator nitroprusside in 10 patients with heart failure. Simultaneous left ventricular micromanometer pressure and radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during atrial natriuretic peptide infusion. The baseline end-systolic pressure-volume relation was generated in nine patients from pressure-volume loops obtained during the two baseline periods and during afterload reduction with nitroprusside. Mean arterial pressure decreased with atrial natriuretic peptide (89 +/- 3 to 80 +/- 2 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (90 +/- 4 to 73 +/- 3 mm Hg, p less than 0.05). Left ventricular end-diastolic pressure also decreased with atrial natriuretic peptide (24 +/- 2 to 16 +/- 3 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (24 +/- 2 to 13 +/- 3 mm Hg, p less than 0.05). Cardiac index increased during infusion of each agent from 2.0 +/- 0.2 to 2.4 +/- 0.2 liters/min per m2 (p less than 0.01). Heart rate increased slightly with nitroprusside but did not change with atrial natriuretic peptide. Peak positive first derivative of left ventricular pressure (dP/dt), ejection fraction and stroke work index were unchanged by either agent. The relation between end-systolic pressure and volume during atrial natriuretic peptide infusion was shifted slightly leftward from the baseline value in four patients, slightly rightward in four and not at all in one patient, indicating no consistent inotropic effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Linearity of the left ventricular end-systolic pressure-volume relation in patients with severe heart failure.

The left ventricular end-systolic pressure-volume relation is a relatively load-independent measure of left ventricular contractile function. Linearity of the relation derived from full left ventricular pressure-volume loops has not previously been demonstrated for patients with severe heart failure. Therefore, nine patients with markedly depressed left ventricular systolic function (ejection fraction 0.14 +/- 0.08) were studied with micromanometer left ventricular pressure measurement and simultaneous radionuclide ventriculography. Afterload was reduced with graded infusions of nitroprusside, allowing construction of pressure-volume loops under four afterload conditions in four patients and three afterload conditions in the other five patients. The end-systolic pressure-volume relation derived from the pressure-volume loops was found to be linear for the range of pressures and volumes examined, with correlation coefficients in individual patients ranging from 0.936 to 0.999 (mean 0.981). The mean slope of the relation (or end-systolic elastance) was 0.71 mm Hg/ml (range 0.42 to 1.52), and the extrapolated volume intercept at zero pressure was positive in all patients. An exponential relation between end-systolic elastance and ejection fraction was demonstrated for this group of patients. Approximations of end-systolic elastance obtained from measurements other than the full pressure-volume loops correlated variably with "true" elastance obtained from the pressure-volume loops. The relation between stroke work and end-diastolic volume was nonlinear in most patients. Thus, the end-systolic pressure-volume relation is linear in the "physiologic" range in patients with severe heart failure. This finding should permit construction of the relation from two loading conditions in clinical studies, facilitating its use as an index of contractile function in patients with heart failure.

Growth factors released into the coronary circulation after vascular injury promote proliferation of human vascular smooth muscle cells in culture.

OBJECTIVES: This study sought to 1) assess in vivo release of platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) into the coronary circulation after vascular injury in human subjects; and 2) evaluate mitogenic effects of PDGF and bFGF on the patient's own vascular smooth muscle cells (VSMCs). BACKGROUND: Circumstantial evidence suggests involvement of PDGF and bFGF peptides in the neointimal response to vascular injury. To date, no study has shown biologically active growth factors within the coronary circulation after vascular injury in human subjects. METHODS: In 18 patients, plasma PDGF AB, platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG) levels were measured in coronary sinus blood obtained before and up to 30 min after angioplasty. In five patients undergoing atherectomy, coronary sinus serum was added to cultured VSMCs derived from atherectomy tissue to assess the mitogenic potential of the serum. Mitogenicity attributable to PDGF and bFGF was determined using neutralizing antibodies to these factors. PDGF A, PDGF B and bFGF were localized within the atherectomy tissue using immunocytochemical analysis. RESULTS: Before angioplasty, PDGF AB, PF4 and beta-TG levels were elevated threefold in patients scheduled for angioplasty compared with those in control patients (p < 0.01). Within 5 min of angioplasty, PDGF AB levels increased twofold and returned toward preangioplasty levels at 30 min; PF4 and beta-TG levels remained elevated. Serum obtained at 30 min after atherectomy showed a sixfold increase in mitogenicity compared with preatherectomy serum (p = 0.01). This increase in mitogenicity was reduced by 20%, 40% and 65% in the presence of neutralizing antibodies to PDGF, bFGF and PDGF + bFGF, respectively. PDGF A, PDGF B and bFGF were visualized within the intima of the atherectomy tissue. CONCLUSIONS: The change in plasma PDGF level is consistent with first-phase release of PDGF after vascular injury. The increase in mitogenicity of serum suggests that PDGF and bFGF are biologically active.

Platelet-monocyte aggregates predict troponin rise after percutaneous coronary intervention and are inhibited by Abciximab.

BACKGROUND: Platelet-monocyte aggregates and other markers of platelet activation were investigated before and after percutaneous coronary intervention (PCI) with abciximab therapy. The study sought to assess the relationship between the level of platelet-monocyte aggregation and increases in cardiac troponin I post coronary intervention. METHODS: Blood samples were collected from 40 patients before PCI and 10 min after abciximab administration. These were tested for platelet activation markers by flow cytometry. Cardiac troponin I levels were assayed at baseline and at 24 h post PCI. RESULTS: Compared to healthy controls, patients with coronary artery disease had elevated markers of platelet activation including platelet-monocyte aggregates, P-selectin and PAC-1 (a marker specific for activated glycoprotein IIb/IIIa) prior to PCI. Increased levels of platelet-monocyte aggregates before PCI were associated with increased expression of P-selectin on the platelet surface. Abciximab therapy reduced platelet-monocyte aggregate levels but had no effect on P-selectin expression. The high levels of expression of activated glycoprotein IIb/IIIa (PAC-1) on platelets prior to PCI was reduced with abciximab therapy. Patients with higher levels of platelet-monocyte aggregates prior to PCI were more likely to develop an elevation of cardiac troponin I during the 24 h after PCI. CONCLUSIONS: Increased levels of platelet-monocyte aggregates may predict patients at risk for troponin elevation following PCI and identify those most likely to benefit from abciximab.

Effects of atrial natriuretic peptide on left ventricular function in hypertension.

Atrial natriuretic peptide (ANP) has natriuretic and vasodilator actions that lower arterial pressure and may be beneficial to hypertensive patients. To assess the effects of ANP on left ventricular function in patients with hypertension, we compared it with the pure vasodilator nitroprusside. Simultaneous left ventricular micromanometer pressure and radionuclide volume were obtained at baseline, during nitroprusside infusion, during a second baseline period, and during ANP infusion in 10 patients with hypertension. Mean arterial pressure fell during ANP and nitroprusside. Heart rate and plasma norepinephrine levels increased by similar amounts during the two agents, whereas cardiac index and stroke volume index were unchanged during both. Peak positive left ventricular dP/dt fell similarly during ANP and nitroprusside, but left ventricular dP/dt at a developed pressure of 40 mm Hg, a less load-dependent index of contractility, was unchanged during both. The relation between end-systolic pressure and volume during ANP infusion was not shifted leftward or rightward from that during nitroprusside infusion, indicating no inotropic effect. Both ANP and nitroprusside shortened at time constant of isovolumic relaxation calculated by the logarithmic method but did not change the time constant calculated by the derivative method. Peak filling rate was unchanged from baseline during both agents. ANP did not shift the end-diastolic pressure-volume point away from the relation constructed from baseline and nitroprusside points. We conclude that ANP has no direct effect on myocardial contractile or diastolic function in patients with hypertension.

Left ventricular diastolic function in patients with left ventricular systolic dysfunction due to coronary artery disease and effect of nicardipine.

To assess the effect of nicardipine on left ventricular (LV) diastolic function independent of concurrent effects on loading conditions in patients with LV systolic dysfunction due to coronary artery disease, equihypotensive doses of intravenous nitroprusside and nicardipine were administered to 12 patients with congestive heart failure due to previous myocardial infarction (LV ejection fraction less than 0.40). LV micromanometer pressure and simultaneous radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during nicardipine infusion. Mean systemic arterial pressure decreased an average of 21 mm Hg with nitroprusside and 19 mm Hg with nicardipine. A greater decrease in LV end-diastolic pressure was observed with nitroprusside (29 +/- 2 to 15 +/- 2 mm Hg, p less than 0.01) than with nicardipine (29 +/- 2 to 25 +/- 3 mm Hg, p less than 0.05). There was a decrease in the time constant of relaxation during nitroprusside but not during nicardipine infusion. There was enough overlap in LV volumes in the baseline and nitroprusside periods to compare diastolic pressure-volume relations over a common range of volumes in 4 patients, and enough overlap in the baseline and nicardipine periods in 11 patients. The relation was shifted downward in 3 of 4 patients taking nitroprusside and in 6 of 11 patients taking nicardipine. The relation between end-diastolic pressure and volume was not shifted with nicardipine.(ABSTRACT TRUNCATED AT 250 WORDS)

A new technique to guarantee access to the sidebranch during bifurcational coronary stenting.

Two consecutive patients are treated using a new technique whereby a stent is implanted across a sidebranch but access to the sidebranch is never lost, thereby guaranteeing further treatment with balloon dilatation or stenting as required.

Failure of current public educational campaigns to impact on the initial response of patients with possible heart attack.

AIMS: The National Heart Foundation of Australia recognizes that the risk of lethal arrhythmias is greater very early after the onset of myocardial infarction and that the more promptly flow can be restored in the infarct-related artery the greater will be the benefits for survival and preservation of heart function. The Heart Foundation has therefore conducted several public media campaigns to encourage patients to seek help more promptly and evaluated their impact. METHODS: Since 1996, we have conducted four surveys of delays preceding admission of patients to coronary care units throughout Australia to assess the impact of the Heart Foundation's media campaigns. Data were collected on 1665 patients who presented to 73 hospitals; information on patient delay was available for 1178 of them. RESULTS: There were no significant differences in patient delay (median 1.5-2.0 h) in the four surveys from 1996 to 2002, nor when patients were categorized by age, sex, presenting diagnosis or history of previous myocardial infarction or coronary revascularization by percutaneous or surgical techniques. CONCLUSION: New approaches are needed to reduce patient-related delay after the onset of symptoms suggesting possible myocardial infarction.

Improving the results of coronary angioplasty.

Coronary angioplasty has changed dramatically in the past three years with major reductions in suboptimal results and restenosis rates, and improvements in safety, efficacy and cost-effectiveness. Intracoronary stent implantation with optimisation of strut expansion and the abandonment of anticoagulants after deployment, have led to less entry-site complications, facilitated early hospital discharge, virtually abolished subacute stent thrombosis and resulted in a 50% reduction in target vessel revascularisation. Adjuvant medical treatment with anti-platelet agents, including glycoprotein IIb/IIIa receptor inhibitors, improves the safety of angioplasty and may further reduce the restenosis rate. Selective use of debulking devices has extended the indications for angioplasty. High resolution fluoroscopy, quantitative coronary angiography and intracoronary ultrasound leading to improved diagnosis, equipment selection and treatment have contributed to better outcomes. Further clinical trials will compare angioplasty and stent implantation with coronary bypass surgery in patients with multivessel coronary disease, and may extend the indications for percutaneous transluminal coronary angioplasty (PTCA) to selected patients with three vessel disease.

Echocardiographic features of a mediastinal pancreatic pseudocyst.

Cross sectional echocardiography detected a mediastinal pancreatic pseudocyst which caused extracardiac compression in a 49 year old man. Computed tomography confirmed the presence of a cystic lesion lying behind the heart and extending from the pancreas to above the carina. Surgical decompression resulted in resolution of the clinical and echocardiographic findings.

Thrombolytic treatment and proteinuria.

OBJECTIVES: To determine whether patients with acute myocardial infarction undergoing thrombolysis with streptokinase develop changes in renal function. DESIGN: Prospective assessment of renal function in 60 consecutive patients admitted with acute myocardial infarction. SETTING: Tertiary referral centre and city general hospital. PATIENTS: 60 consecutive patients with acute myocardial infarction. Thirty eight were given streptokinase and 17 tissue plasminogen activator (alteplase) and five no thrombolytic agent (non-streptokinase group). MAIN OUTCOME MEASURES: Proteinuria and creatinine clearance on admission (day 1) and on days 3 and 6; serum urea and creatinine concentrations on days 1 and 7; streptokinase IgG on days 1, 2, and 7. RESULTS: Significant proteinuria (> 0.15 g/24 h) was found in 31 (82%) of the 38 patients in the streptokinase group (mean 0.47 g/24 h (95% confidence interval 0.35 to 0.6 g/24 h)) in the 24 hours after admission compared with six (27%) out of 22 in the non-streptokinase group (mean 0.17 g/24 h (0.12 to 0.2 g/24 h); P = 0.008). In the streptokinase group this decreased to the normal range by day 3 (mean 0.15 g/24 h (0.1 to 0.22 g/24 h); P = 0.0001 v baseline). Electrophoresis of urine showed the proteinuria to be glomerular in origin. Creatinine clearance and serum creatinine and urea concentrations were similar in both groups. In the streptokinase group detectable streptokinase IgG titres were found in 28 out of 32 (87%) patients. The median titre on admission was 16 (range 0-110); it fell to 3 (range 0-80; P = 0.001) by day 2 and increased to 61 (range 0-7700; P = 0.0002 v baseline) by day 7. CONCLUSIONS: Streptokinase was associated with significant early onset proteinuria of glomerular origin. This started to resolve by day 3 and resulted in no deterioration in overall renal function. The temporal relation to the initial fall in antibody titre suggests that it could be the result of immune complex deposition in the glomeruli.

Percutaneous transluminal coronary angioplasty in a 30-month-old child with embolic long segment occlusion of the left anterior descending artery.

A 30-mo-old girl developed occlusion of her left anterior descending coronary artery following mitral valve replacement. She presented with refractory angina pectoris. Successful percutaneous transluminal coronary angioplasty of the left anterior descending artery was performed, resulting in restoration of flow, resolution of anginal symptoms, and early improvement in left ventricular function.

Thrombosis of a mechanical tricuspid valve prosthesis and of the left subclavian vein: successful therapy with thrombolysis.

A patient with thrombosis of a mechanical prosthetic valve in the tricuspid position, simultaneous extensive left subclavian vein thrombotic occlusion, and pulmonary embolism is successfully treated with a urokinase infusion delivered using catheter-based techniques.