Testicular germ cell tumours are the most common malignancy in men aged 20 to 40 years. They are subdivided into seminoma and non-seminomatous germ cell tumours (NSGCTs). Both seminoma and NSGCT occur at about the same rate, however some tumours contain a combination of both. Cisplatin-based chemotherapy is used adjuvantly in high-risk stage 1 mixed and NSGCT patients and contributes towards oncological cure in almost all metastatic cases, regardless of histology. However, cardiovascular toxicity is a major concern. In addition to acute endothelial toxicity and associated risk of arterial thrombosis, accelerated atherosclerosis may be the result of chemotherapy-associated latent cardio-metabolic dysfunction. A 45-year-old man began treatment with cisplatin-based chemotherapy for testicular cancer. On day 9, he suffered an anterior ST segment elevation myocardial infarction (STEMI). There was proximal occlusion of the left anterior descending (LAD) artery but otherwise normal coronary arteries. Ten months following chemotherapy, he had another STEMI. There was a fresh obstructive lesion in the previously angiographically normal mid LAD, new diffuse coronary atheroma elsewhere and a deterioration in lipid profile despite statin therapy. Acute and longer-term cardiovascular risks of cisplatin-based chemotherapy may have different underlying pathophysiological mechanisms. These issues are of growing relevance in a population of patients expected to have excellent cancer-related outcomes.

Objective We hypothesised that, compared with culprit-only primary percutaneous coronary intervention (PCI), additional preventive PCI in selected patients with ST-elevation myocardial infarction with multivessel disease would not be associated with iatrogenic myocardial infarction, and would be associated with reductions in left ventricular (LV) volumes in the longer term. Methods In the preventive angioplasty in myocardial infarction trial (PRAMI; ISRCTN73028481), cardiac magnetic resonance (CMR) was prespecified in two centres and performed (median, IQR) 3 (1, 5) and 209 (189, 957) days after primary PCI. Results From 219 enrolled patients in two sites, 84% underwent CMR. 42 (50%) were randomised to culprit-artery-only PCI and 42 (50%) were randomised to preventive PCI. Follow-up CMR scans were available in 72 (86%) patients. There were two (4.8%) cases of procedure-related myocardial infarction in the preventive PCI group. The culprit-artery-only group had a higher proportion of anterior myocardial infarctions (MIs) (55% vs 24%). Infarct sizes (% LV mass) at baseline and follow-up were similar. At follow-up, there was no difference in LV ejection fraction (%, median (IQR), (culprit-artery-only PCI vs preventive PCI) 51.7 (42.9, 60.2) vs 54.4 (49.3, 62.8), p=0.23), LV end-diastolic volume (mL/m2, 69.3 (59.4, 79.9) vs 66.1 (54.7, 73.7), p=0.48) and LV end-systolic volume (mL/m2, 31.8 (24.4, 43.0) vs 30.7 (23.0, 36.3), p=0.20). Non-culprit angiographic lesions had low-risk Syntax scores and 47% had non-complex characteristics. Conclusions Compared with culprit-only PCI, non-infarct-artery MI in the preventive PCI strategy was uncommon and LV volumes and ejection fraction were similar.

Background In the Randomised Trial of Preventive Angioplasty in Myocardial Infarction (PRAMI; ISRCTN73028481), compared with infarct-related artery (IRA)-only PCI, additional immediate multivessel PCI (MV-PCI) of non-IRA lesions in patients with acute ST elevation myocardial infarction (STEMI) and multivessel coronary disease (MVD) improved long term prognosis. We studied left ventricular (LV) outcomes in a pre-specified cardiac magnetic resonance (CMR) sub-study. Methods In a single centre prospective sub-study, PRAMI participants were invited to undergo CMR at 1.5 Tesla 1 week and 1 year after primary PCI. LV volumes and function were analysed using semi-automated software by a clinician blinded to treatment group assignment and clinical outcomes. The statistical analyses were performed by an independent statistician. Results Of 465 randomised trial participants in 6 UK hospitals, 138 (30%) were enrolled in Glasgow. Eighty patients (17%) (mean age 60 years, 76% male) underwent CMR initially (n = 41 (51%) in the multi-vessel PCI group; n = 39 (49%) in the IRA-only group). 69 (86%) of these patients had a follow up CMR scan at 1 year (n = 7 lost to follow-up, n = 4 deceased). Mean (and SD) LVEF and volumes at 1 week post-MI and their change at 1 year from baseline were similar (Table 1). Conclusion The CMR sub-study participants represented the majority of all randomised participants in our hospital, which included one third of the PRAMI trial population. Random treatment group assignment in this CMR study was evenly balanced. LV function and volumes were similar at 1 week and 1 year post-intervention in survivors. The CMR sub-study suggests that the benefit of the preventive PCI strategy in PRAMI may not be mediated by any effects on LV function and remodelling. Funding Golden Jubilee National Hospital; PRAMI was funded by Barts and the London Charity.

An 81-year-old woman with myeloma and a recent fractured femoral neck presented after a collapse. On arrival, she was tachycardic, hypotensive, and hypoxic. ECG showed incomplete right bundle branch block, prominent S waves in lead I, Q waves and T-wave inversion in lead III (Figure A, black arrows). Echocardiography, performed by a cardiologist in the emergency department (ED), revealed classic features of massive pulmonary thromboembolism, with right ventricle enlargement and regional impairment of the right ventricle free wall (McConnell’s sign) (Figure B; Video E1, available online at http://www.annemergmed.com),1McConnell M.V. Solomon S.D. Rayan M.E. et al.Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism.Am J Cardiol. 1996; 78: 469-473Abstract Full Text Full Text PDF PubMed Scopus (564) Google Scholar compression of the left ventricle, and a large serpentine thrombus in the right atrium, which extends into the right ventricle (Figure B, white arrow; Video E1, available online at http://www.annemergmed.com). Less than 2 minutes after thrombolysis, the thrombus mobilized to the right ventricle (Figure D, white arrow; Video E2, available online at http://www.annemergmed.com) and then to the lungs (Video E3, available online at http://www.annemergmed.com), with resultant hemodynamic collapse with loss of peripheral pulses and an unrecordable blood pressure. The patient transiently became more hypoxic but did not require intubation, and after aggressive fluid resuscitation and inotropic support, hemodynamic stability was restored during 30 minutes. Massive bilateral pulmonary thromboembolisms were later confirmed on computed tomography (Figure C, white arrows). The patient made a full recovery and was discharged home after being established on oral anticoagulation. Massive pulmonary embolism. Current guidelines advocate the use of bedside echocardiography in the critically unwell patient because positive findings like those described above can confirm the diagnosis and justify early thrombolysis, where absence of echocardiographic signs in the shocked patient practically excludes pulmonary thromboembolism as the cause of hemodynamic compromise.2Torbicki A. Perrier A. Konstantinides S. et al.Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC).Eur Heart J. 2008; 29: 2276-2315Crossref PubMed Scopus (8) Google Scholar This case highlights the utility of bedside echocardiography, although ultimately treatment was delayed by more than 1 hour in this case because a cardiologist was required to perform the scan. Thereafter, treatment was prompt, with thrombolysis delivered within 5 minutes of the echocardiogram being performed. Perhaps more widespread training and use of echocardiography in the ED would facilitate early treatment of similar patients. eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiIxZjBjMDczODhiMzgzN2Q3YmViMDUyODcyNjg1YWM5NCIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjk2OTk5NDA4fQ.sGH3Ah4uzt8vTaBuQdtHlT6bwW9uWdy3EPjRzrEnhMSie5T4qQY6EtctO1iZavbdb4-NShUbVEvA89QdunBfG1pwHDuV_dLSYdD7lvkiOZJauG_6UKu3hok8mxoN2yxO8mdK3hj1G1aPp-mvq2cautdbH8IHByhKyCpXndsEult8RuzehVWxkKwFHVKMOYERe0kmLEAT_pZlL9dsTvdsuuvjHYrA6tTaoWAAO5AV7jBi6uSElKRu-tVLG0ZofJFbEPpMvebbbsvrx5Be9E2GHz-H9Yi9HTYfpW0xCRqICVax5hx-16NHLIVTEOwysype8vGARDymaVISFv85NwVMPQ Download .mp4 (1.6 MB) Help with .mp4 files Video E1Apical four chamber echocardiogram pre-thrombolysis showing mobile thrombus in right atrium.eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiI3ZTRiYmJiMjllYzg3OTIwZmJkYzc5NmM1MmI2MGQ5MSIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjk2OTk5NDA4fQ.CV70iAuRuz8atjxVf7E4b49wxlQRLISbpYp2TsbL7d0lbzk7YRD2N5j67Z7-1e8DSA3eEwsJqHJAI7uJLvnZXxOZzheHVIoFwCcGRtHoHAfkC7dg5jo_7axf0kVTepZ3rQu4fW_uYNpCrmKa3ArUTguiHu08v65lkjHhzqnit4kDXa0GmDzkITMTwgEScV2m8nfvaSvAx6tt6TpQx9Wc1suhaZAbMANmCckF03XJ5rEPunZfTKK_Nsz5ZHTYTTxrs2W_iSNRdr7RnJ5NPKh6_F_y0MuZJgoGQsQ1NsfRIoZYU9ZV_AWmW083REcSdyjQqRuvJSk7IrAYYkhJPIYJ5w Download .mp4 (2.11 MB) Help with .mp4 files Video E2Apical four chamber echocardiogram during thrombolysis demonstrating mobilzation of thrombus from right atrium to right ventricle.eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiIwYThjNDE0MWMwZWViNTJmMjU2OWY5ZDVmMGJjZTlkMSIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjk2OTk5NDA4fQ.V2U0FMw0SgvXuIsMy8w6GbCpXVAhdOw7JSjyBK95DjFv8sghcWOsySo-hLFJbeLYAhiR5pORLxuN7i8NuqpkbRXtIyVMnLKjovYbQa1rz0NWY2rQu-zM8yUlbqg48ZyBy1ZWGNrx8uHOAk-2G4CuCg_8g6y4k8iGFDID0GX1mMUCRQ9Fv1qQjNGAYXwOHVDuWFcrNGYcmtdH5_eIiwd28sm7G6dL07LvRnYXTiGpEP_X288cfzMXrZP5nV29UpfgNIHMXnd_8NDnQFC9PujjIuyL0eEpGY5SRRgcEcnnoK6f1QDREDGQcPn554I9fRqOvQTAVy44LjFcw0pH4a_bEw Download .mp4 (1.09 MB) Help with .mp4 files Video E3Apical four chamber echocardiogram showing mobilization of thrombus from right ventricle to pulmonary artery following thrombolysis.

Background: T2-weighted cardiovascular magnetic resonance (CMR) is clinically-useful for imaging the ischemic area-at-risk and amount of salvageable myocardium in patients with acute myocardial infarction (MI). However, to date, quantification of oedema is user-defined and potentially subjective.Methods: We describe a highly automatic framework for quantifying myocardial oedema from bright blood T2-weighted CMR in patients with acute MI. Our approach retains user input (i.e. clinical judgment) to confirm the presence of oedema on an image which is then subjected to an automatic analysis. The new method was tested on 25 consecutive acute MI patients who had a CMR within 48 hours of hospital admission. Left ventricular wall boundaries were delineated automatically by variational level set methods followed by automatic detection of myocardial oedema by fitting a Rayleigh-Gaussian mixture statistical model. These data were compared with results from manual segmentation of the left ventricular wall and oedema, the current standard approach.Results: The mean perpendicular distances between automatically detected left ventricular boundaries and corresponding manual delineated boundaries were in the range of 1-2 mm. Dice similarity coefficients for agreement (0=no agreement, 1=perfect agreement) between manual delineation and automatic segmentation of the left ventricular wall boundaries and oedema regions were 0.86 and 0.74, respectively.Conclusion: Compared to standard manual approaches, the new highly automatic method for estimating myocardial oedema is accurate and straightforward. It has potential as a generic software tool for physicians to use in clinical practice.

Background The pathophysiology of myocardial injury and repair in patients with ST‐elevation myocardial infarction is incompletely understood. We investigated the relationships among culprit artery microvascular resistance, myocardial salvage, and ventricular function. Methods and Results The index of microvascular resistance (IMR) was measured by means of a pressure‐ and temperature‐sensitive coronary guidewire in 108 patients with ST‐elevation myocardial infarction (83% male) at the end of primary percutaneous coronary intervention. Paired cardiac MRI (cardiac magnetic resonance) scans were performed early (2 days; n=108) and late (3 months; n=96) after myocardial infarction. T 2 ‐weighted‐ and late gadolinium–enhanced cardiac magnetic resonance delineated the ischemic area at risk and infarct size, respectively. Myocardial salvage was calculated by subtracting infarct size from area at risk. Univariable and multivariable models were constructed to determine the impact of IMR on cardiac magnetic resonance–derived surrogate outcomes. The median (interquartile range) IMR was 28 (17–42) mm Hg/s. The median (interquartile range) area at risk was 32% (24%–41%) of left ventricular mass, and the myocardial salvage index was 21% (11%–43%). IMR was a significant multivariable predictor of early myocardial salvage, with a multiplicative effect of 0.87 (95% confidence interval 0.82 to 0.92) per 20% increase in IMR; P <0.001. In patients with anterior myocardial infarction, IMR was a multivariable predictor of early and late myocardial salvage, with multiplicative effects of 0.82 (95% confidence interval 0.75 to 0.90; P <0.001) and 0.92 (95% confidence interval 0.88 to 0.96; P <0.001), respectively. IMR also predicted the presence and extent of microvascular obstruction and myocardial hemorrhage. Conclusion Microvascular resistance measured during primary percutaneous coronary intervention significantly predicts myocardial salvage, infarct characteristics, and left ventricular ejection fraction in patients with ST‐elevation myocardial infarction. ( J Am Heart Assoc . 2012;1:e002246 doi : 10.1161/JAHA.112.002246 )

Background— Myocardial hemorrhage after myocardial infarction (MI) usually goes undetected. We investigated the diagnostic accuracy of bright-blood T 2 -weighted cardiac MRI for myocardial hemorrhage in experimental MI. Methods and Results— MI was created in swine by occluding the left anterior descending (n=10) or circumflex (n=5) coronary arteries for 90 minutes followed by reperfusion for ≤3 days (n=2), 10 days (n=7), or 60 days (n=6). MRI was performed at 1.5 T, using bright-blood T 2 -prepared steady-state free-precession, T 2 * and early (1 minute) and late (10–15 minutes) gadolinium enhancement (EGE, LGE, respectively) MRI. Left ventricular sections and histology were assessed for hemorrhage by an experienced cardiac pathologist blinded to the MRI data. Hypointense regions on T 2 -weighted and contrast-enhanced MRI were independently determined by 3 cardiologists experienced in MRI who were also blinded to the pathology results. Eighty ventricular pathological sections were matched with MRI (n=68 for EGE MRI). All sections with evidence of MI (n=63, 79%) also exhibited hyperintense zones consistent with edema on T 2 -weighted MRI and infarct on LGE MRI. Myocardial hemorrhage occurred in 49 left ventricular sections (61%) and corresponded with signal voids on 48 T 2 -weighted (98%) and 26 LGE-MRI (53%). Alternatively, signal voids occurred in the absence of hemorrhage in 3 T 2 -weighted (90% specificity) and 5 LGE MRI (84% specificity). On EGE MRI, 27 of 43 cases of early microvascular obstruction corresponded with hemorrhage (63% sensitivity), whereas 5 of 25 defects occurred in the absence of hemorrhage (80% specificity). The positive and negative predictive values for pathological evidence of hemorrhage were 94% and 96% for T 2 -weighted, 84% and 55% for LGE MRI, and 85% and 56% for EGE MRI. Conclusions— Bright-blood T 2 -weighted MRI has high diagnostic accuracy for myocardial hemorrhage.

BACKGROUND:Twelve-lead electrocardiography is a standard preoperative investigation for patients undergoing major surgery. There is uncertainty and debate over the usefulness of this test for stratifying postoperative cardiac risk. The aim of this study was to investigate the correlation between an abnormal electrocardiogram (ECG) and the postoperative cardiac event rate. METHODS:A prospective single-center observational cohort study in patients undergoing major noncardiac surgery was performed. ECGs were analyzed at the end of the study by a cardiologist and a clinician blinded to the clinical outcomes. The primary endpoints were a major adverse cardiac event (MACE), defined as nonfatal myocardial infarction or cardiac death, and perioperative mortality. RESULTS:A total of 345 patients were included, who had undergone aortic surgery 25.8%, lower limb bypass 29.0%, amputation 25.2%, or laparotomy 20.0%. An abnormal ECG was present in 141 (40.9%) patients. MACE occurred in 46 (13.3%) cases. Patients with an abnormal ECG had a significantly higher incidence of MACE (21.6 vs. 8.3%, P < 0.001). Multivariate analysis showed that left ventricular strain and a prolonged QTc interval (>440 ms) were independent predictors of postoperative adverse events. Among patients with no prior history of ischemic heart disease, those with an abnormal ECG had a higher MACE rate (20.3%) than those patients with a normal ECG (8.6%) (P = 0.01). CONCLUSION:Preoperative electrocardiography is a useful screening test for predicting perioperative cardiac events. Patients with an abnormal ECG but without a prior history of heart disease are a high-risk group potentially amenable to intervention and risk reduction.

Background— T2-Weighted MRI reveals myocardial edema and enables estimation of the ischemic area at risk and myocardial salvage in patients with acute myocardial infarction (MI). We compared the diagnostic accuracy of a new bright-blood T2-weighted with a standard black blood T2-weighted MRI in patients with acute MI. Methods and Results— A breath-hold, bright-blood T2-weighted, Acquisition for Cardiac Unified T2 Edema pulse sequence with normalization for coil sensitivity and a breath-hold T2 dark-blood short tau inversion recovery sequence were used to depict the area at risk in 54 consecutive acute MI patients. Infarct size was measured on gadolinium late contrast enhancement images. Compared with dark-blood T2-weighted MRI, consensus agreements between independent observers for identification of myocardial edema were higher with bright-blood T2-weighted MRI when evaluated per patient ( P <0.001) and per segment of left ventricle ( P <0.001). Compared with bright-blood T2-weighted MRI, dark-blood T2-weighted MRI underestimated the area at risk compared with infarct size ( P <0.001). The 95% limits of agreement for interobserver agreements for the ischemic area at risk and myocardial salvage were wider with dark-blood T2-weighted MRI than with bright-blood T2-weighted MRI. Bright blood enabled more accurate identification of the culprit coronary artery with correct identification in 94% of cases compared with 61% for dark blood ( P <0.001). Conclusions— Bright-blood T2-weighted MRI has higher diagnostic accuracy than dark-blood T2-weighted MRI. Additionally, dark-blood T2-weighted MRI may underestimate area at risk and myocardial salvage.

Introduction: Circulating injury and repair pathways in human myocardial infarction (MI) are incompletely understood. We investigated rheological and regenerative pathways acutely and in the longer term post-MI. Methods: Blood constituents implicated in myocardial injury (e.g. red cell volume distribution width, hemoglobin) and repair (circulating CD34 + progenitor cells, serum vascular endothelial growth factor (VEGF), serum thymosin β 4 and AcSDKP excreted in urine) were quantified in patients 2 days and 3 months after ST elevation MI (STEMI). Coronary collateral flow was measured invasively during emergency percutaneous coronary intervention. Cardiac function and remodeling were quantified by gadolinium contrast enhanced MRI at 1.5T at these time-points. Results: Thirty-five consecutive STEMI patients (mean±SD age 58±10 years; 3(9%) women) were included. Mean (SD) thymosin β 4 concentration was lower at day 2 compared to at 3 months post-MI (3.0±1.6 vs. 7.0±2.9 μ g/L; P<0.0001). Two days post-MI, AcSDKP correlated negatively with white cell count (R=−0.54; P=0.024) and VEGF (R=−0.57; P=0.038). After adjustment for white cell count, AcSDKP two days post-MI negatively predicted left ventricular (LV) ejection fraction (R 2 =0.43; P=0.024) and positively predicted LV end-systolic volume index (R 2 =0.56; P=0.011) at 3 months. At follow-up, CD34 + count negatively predicted myocardial infarct mass (R 2 =0.29; P=0.015) and LV end-systolic volume index (R 2 =0.20; P=0.02). Delta CD34 + negatively predicted infarct mass (R 2 =0.13; P=0.049) at 3 months. Mean red cell volume at day 2 negatively predicted LV end-systolic volume index (R 2 =0.24; P=0.038) and infarct size (R 2 =0.13; P=0.045) at 3 months. In multivariable analyses, VEGF at day 2 predicted LV end-diastolic volume index at follow-up (coefficient of variation (95% CI) −0.021 (−0.038, −0.035); P=0.021). Coronary collateral supply was negatively predicted by hemoglobin (−0.04 (−0.06, −0.11); P=0.006) and positively predicted by red cell volume distribution width (0.06 (0.02, 0.10); P=0.004) and platelet count (0.001 (0.0001, 0.002); P=0.001) at day 2. Conclusions: Circulating injury/repair responses predict coronary collateral recruitment and cardiac function and remodeling post-MI.