Pawel Rostoff

Life-threatening cardiac manifestations of primary antiphospholipid syndrome

We report a rare case of primary antiphospholipid syndrome (APS) in a 43-year-old man presenting as recurrent acute coronary stent thrombosis and complicated by three myocardial infarctions. As illustrated in this report, in APS patients recurrent life-threatening arterial thrombotic events may occur in spite of recommended anticoagulant therapy. We conclude that the APS should be considered as a potential cause of acute coronary syndrome, particularly in young individuals with a history of recurrent thrombotic events and/or with abnormal coagulation test results. Further studies are needed to determine the best therapeutic strategy for APS patients with acute coronary syndrome.

Transient ST-segment elevation in lead aVR associated with tako-tsubo cardiomyopathy

ST-segment elevation in lead aVR in patients with angina at rest can be related to transmural ischemia of the basal part of the interventricular septum, frequently due to left main or multivessel coronary disease. However, this electrocardiographic (ECG) sign may also occur in other clinical conditions manifesting by acute chest pain. We present a case of a 76-year-old Caucasian woman with transient ST-segment elevation in lead aVR associated with tako-tsubo cardiomyopathy. Our report seems to confirm the hypothesis about the role of reversible myocardial ischemia involving the basal part of the interventricular septum in the pathogenesis of tako-tsubo cardiomyopathy. In conclusion, ST-segment elevation in lead aVR in patients with a clinical presentation of acute coronary syndrome may be not related to coronary artery disease. Tako-tsubo cardiomyopathy should be considered among the causes of ST-segment elevation in lead aVR in patients with angina at rest. Further studies are needed to evaluate the occurrence and importance of this ECG sign in patients with tako-tsubo cardiomyopathy.

Stenotrophomonas maltophilia pacemaker endocarditis in a patient with d-transposition of the great arteries after atrial switch procedure

We report a case of pacemaker endocarditis due to Stenotrophomonas maltophilia in a 22-year-old Caucasian man with d-transposition of the great arteries after atrial switch procedure. S.maltophilia isolated from blood cultures was susceptible to trimethoprim-sulfamethoxazole and amikacin, and resistant to ciprofloxacin and all tested β-lactam antibiotics. The infected pacemaker system was completely removed by thoracotomy. Simultaneously, a new DDD pacemaker and epicardial electrodes were successfully implanted and selective antibiotic therapy consisting of trimethoprim-sulfamethoxazole (480xa0mg i.v. q 6xa0h) and amikacin (250xa0mg i.v. twice daily) was continued. However, the post-operative course was complicated by septic shock and the patient died on 9th day after surgery. Importantly, S.maltophilia isolated from extracted pacemaker leads was multidrug-resistant including to trimethoprim-sulfamethoxazole, ciprofloxacin, all tested aminoglycosides, and β-lactams, with the exception of ticarcillin-clavulanate. In conclusion, pacemaker endocarditis due to Stenotrophomonas maltophilia is an extremely rare but serious complication of permanent pacing therapy. The susceptibility of S.maltophilia isolates to antimicrobial agents can change during the course of infection. Despite the inherent resistance of S.maltophilia to most β-lactam antibiotics, multidrug-resistant strains may be susceptible in vitro to ticarcillin-clavulanate. Further studies are needed to determine the optimal management of patients with pacemaker endocarditis caused by Stenotrophomonas maltophilia.

Ergotamine-induced cardiovascular toxicity: mechanisms and clinical significance.

concluded that an acute elevation of pulmonary capillary wedge pressure does not limit exercise capacity in CHF. In other words a patient could have a very high PCWP but a relatively good oxygen uptake. According to this Fink et al. did not found an improvement of ventilatory efficiency by acute lowering of filling pressures [9]. Our data confirm that the acute cardiac output response is the main central hemodynamic determinant of exercise capacity and not acute pressure changes. Central cardiac pressures derived from PACmeasurements cannot be deduced from the results of a CPX test and may add independent information during the evaluation of heart failure patients. We hypothesize that a subgroup of patients for example with a disparity between symptoms and results of non-invasive tests may profit from PAC procedures. A prospective study on the impact on prognosis of different non-invasive and invasive hemodynamic tests in patients with severe heart failure is warranted.

Trauma-induced acute myocardial infarction due to delayed dissection of the left anterior descending coronary artery

Acute myocardial infarction is a very rare, life-threatening complication of blunt chest trauma. A 27-year-old man with no previous medical history was admitted to the emergency department due to multiple trauma following a car accident. After 48h following the accident, the patients condition rapidly deteriorated, with severe dyspnea at rest, tachycardia, and increasing chest pain. A 12-lead ECG showed a sinus tachycardia at 120bpm with significant ST-segment elevation in leads V1 to V5, pathologic Q wave in I, aVL, and QS complex in leads V1 to V4. Bedside echocardiography disclosed akinesis of the anterior and lateral walls, apex, and anterior septum with severely decreased left ventricular ejection fraction of 30%. Urgent coronary angiography revealed an occlusive dissection of the proximal left anterior descending coronary artery. Primary percutaneous coronary intervention with a Biolimus A9™-eluting stent implantation were successfully performed. The further course was uneventful. At 12-month follow-up, the patient has remained asymptomatic with no recurrence of cardiovascular symptoms.

Relationship between polyunsaturated fatty acid composition in serum phospholipids, systemic low-grade inflammation, and glycemic control in patients with type 2 diabetes and atherosclerotic cardiovascular disease

BackgroundThere are inconsistent data about the role of serum phospholipid fatty acid composition in patients with type 2 diabetes (T2DM) and atherosclerotic cardiovascular disease (ASCVD). The aim of the study was to investigate the relationship between serum phospholipid fatty acid composition, systemic low-grade inflammation, and glycemic control in high-risk T2DM patients.MethodsSeventy-four patients (26% women, mean age 65.6xa0±xa06.8xa0years) with T2DM (median diabetes duration 10xa0years) and documented ASCVD (74 with coronary artery disease, 26 with peripheral arterial disease) were enrolled in the study. Baseline HbA1c was estimated using turbidimetric inhibition immunoassay. According to the median value of HbA1c the patients were grouped into those with HbA1cxa0<xa07.0% (<xa053xa0mmol/mol) (nxa0=xa038) and those with HbA1cxa0≥xa07.0% (≥xa053xa0mmol/mol) (nxa0=xa036). Serum phospholipid fatty acids were measured with gas chromatography.ResultsPatients with HbA1cxa0≥xa07.0%, compared with those with HbA1cxa0<xa07.0% had similar composition of saturated and monounsaturated fatty acids in serum phospholipids, but had higher concentrations of linoleic acid (LA) and higher n-6/n-3 polyunsaturated fatty acid (PUFA) ratio as well as lower levels of eicosapentaenoic acid (EPA), total n-3 PUFAs, and the EPA/arachidonic acid ratio. We found that LA (rxa0=xa00.25; pxa0=xa00.03) and n-6/n-3 PUFA ratio (rxa0=xa00.28; pxa0=xa00.02) were positively correlated with HbA1c. Multivariate logistic regression analysis showed that n-6/n-3 PUFA ratio, hsCRP and T2DM duration were independent predictors of worse glycemic control in patients with T2DM and ASCVD.ConclusionsThis study showed that glycemic control in high-risk T2DM patients with ASCVD was significantly associated with unfavorable serum phospholipid n-6/n-3 PUFA ratio and greater systemic inflammation.

Fulminant adrenergic myocarditis complicated by pulmonary edema, cardiogenic shock and cardiac arrest

Adrenergic myocarditis is an uncommon presentation of pheochromocytoma and extremely rare cause of de novo acute heart failure (AHF). We present a case of a 31-year-old Caucasian woman with a history of hypertension and recurrent occipital headaches who was admitted to the emergency department due to severe de novo AHF presenting as pulmonary edema and cardiogenic shock. During the hospital admission the patient experienced asystolic cardiac arrest and was successfully resuscitated, intubated, and mechanically ventilated. Bedside transthoracic echocardiography revealed severe diffuse left ventricular hypokinesis with ejection fraction (LVEF) of 10%. Coronary angiography disclosed normal epicardial coronary arteries. The diagnosis of fulminant myocarditis was based on clinical, laboratory and imaging findings including cardiac magnetic resonance imaging (cMRI) Lake Louise criteria. STIR-cMRI sequences revealed myocardial edema in the lateral, inferior and posterior walls of the left ventricle, whereas T1-weighted early contrast-enhanced sequences showed myocardial hyperemia and capillary leak. An ultrasound and computed tomographic scan of the abdomen disclosed a solid, heterogeneous mass (3.6×3.2×2.8-cm) in the right suprarenal area. Urinary and plasma catecholamines and metanephrines were markedly elevated. A pheochromocytoma was suspected and laparoscopic resection of the tumor was performed after pharmacological preparation with phenoxybenzamine. The histopathological findings were consistent with pheochromocytoma. Follow-up cMRI showed complete reversal of myocardial edema and hyperemia. At 12-month follow-up, the patient has remained asymptomatic and normotensive with no recurrence of cardiovascular symptoms.