Safety of therapeutic hypothermia in post VF/VT cardiac arrest patients.

Therapeutic hypothermia (TH) is a process of cooling a patient post ventricular tachycardia/ventricular fibrillation (VT/VF) cardiac arrest to 32-34 degrees C for 24 hours. This improves neurological outcome and is part of current guidelines. Hypothermia prolongs QT interval, which can precipitate torsades de pointes (TdP). We performed a retrospective review of all patients who received TH in our hospital over a period of 2 years to assess the effect of TH on the corrected OT interval (QTc) and any possible pro-arrhythmia. A total of 13 patients received TH. QTc prolonged in all patients with an average of 80.3 + 57.2 ms., and up to 109.8 + 80.4 ms in patients who received Amiodarone concurrently. No TdP was seen in any patient. We conclude that TH is safe, though careful monitoring of the OTc interval is advisable especially with concurrent use of QT prolonging drugs.

Resource utilisation for syncope presenting to an acute hospital Emergency Department.

BACKGROUND: Syncope is a common clinical problem accounting for up to 6% of hospital admissions. Little is known about resource utilisation for patients admitted for syncope management in Ireland. AIM: To determine the utilisation of resources for patients admitted for syncope management. METHODS: Single centre observational case series of consecutive adult patients presenting to an acute hospital Emergency Department with syncope over a 5-month period. RESULTS: Two-hundred and fourteen of 18,898 patients (1.1%) had a syncopal episode, 110 (51.4%) of whom were admitted. Mean length of stay was 6.9 days. Sixty-four of these admissions were deemed unnecessary by retrospective review when compared to ESC guidelines. Eighty-five (77.3%) admitted patients had cardiac investigations and 56 (51%) had brain imaging performed. CONCLUSIONS: Syncope places a large demand on overstretched hospital resources. Most cases can be managed safely as an outpatient and to facilitate this, hospitals should develop outpatient Syncope Management Units.

Multivessel coronary thrombosis resulting from heparin induced thrombocytopenia.

Thrombosis associated with a drop in the platelet count may occur in 33-50% of the patients who develop heparin-induced thrombocytopenia (HIT) during treatment with unfractionated heparin. We report the case of a 63-year-old man who was treated with unfractionated heparin following a non-ST segment elevation myocardial infarction (NSTEMI). He developed an acute ST segment elevation infarction (STEMI) on day 3 with an associated severe thrombocytopenia. He was successfully treated with percutaneous intervention and aspiration of coronary thrombus from the right coronary artery and the left circulflex artery, followed by an infusion a direct thrombin inhibitor lepirudin/bivalirudin. He made an excellent recovery.

The radial artery: an alternative access site for diagnostic and interventional coronary procedures.

BACKGROUND: Percutaneous techniques are routinely used in the diagnosis and treatment of cardiovascular disease. The transfemoral route is the most frequently used arterial access site for performing these procedures AIM: To describe a technique to gain arterial access via the radial artery to perform diagnostic and invasive procedures. METHODS: Patient selection is key to establishing a successful transradial service. RESULTS: There is a significant vascular complication rate when using the transfemoral route. Transfemoral access can also be difficult in patients with peripheral vascular disease. Arterial access via the right radial artery represents a realistic alternative to the transfemoral route for performing diagnostic and therapeutic coronary procedures. CONCLUSIONS: The radial artery offers a safe and effective alternative access site for performing diagnostic and interventional coronary procedures. The need for alternatives to femoral artery access is critical in patients with severe peripheral vascular disease. The establishment and ongoing provision of radial artery intervention allows for a significant reduction in major vascular complication rates, earlier patient ambulation, increased patient comfort and the potential to establish day case coronary intervention.

A rapid agglutination assay to detect anti-streptokinase antibodies.

BACKGROUND: Streptokinase resistance may cause suboptimal thrombolytic therapy. AIM: To develop a rapid latex-bead assay to detect streptokinase antibodies. METHODS: Sera were obtained from 16 patients presenting with acute myocardial infarction (MI) before treatment with streptokinase and 1 and 6 months post treatment, and from 100 controls. Sera were assayed for anti-streptokinase antibodies using a functional streptokinase-neutralising assay. RESULTS: Streptokinase-neutralising activity was low in controls (54 +/- 5U/ml) and patients prior to treatment (101 +/- 18), increasing to 2,110 +/- 823 and 1,017 +/- 169 at 1 and 6 months (mean +/- SEM). The latex assay had a sensitivity of 94% and a specificity of 93% for detecting individuals with > 350U/ml of streptokinase resistance, which is sufficient to neutralise the drug clinically. CONCLUSIONS: Estimation of streptokinase resistance using an enzyme immunoassay and a latex bead assay correlated well with serum neutralising activity. This assay can rapidly identify patients who have a high level of streptokinase-neutralising activity.

Inflammatory markers as predictors of clinical outcome in acute coronary syndromes.

Inflammation is a critical pathogenic component in acute coronary syndromes. As a consequence the potential use of inflammatory markers as predictors of clinical outcome in acute coronary syndromes has been investigated. This review outlines the pathology underlying acute coronary syndromes and reviews the published data on inflammatory markers in acute coronary syndromes.

Inflammation in acute coronary syndromes.

Extensive evidence supports a pathogenic role for both local and systemic inflammation in acute coronary syndromes. However, several important questions remain unanswered. Is the observed inflammatory process a precursor or a consequence of coronary plaque rupture? Is the inflammatory component of unstable coronary disease a potential therapeutic target? Finally, do infectious agents have a pathogenic role in coronary atherosclerosis and acute coronary syndromes?

Assessing the risk of sudden cardiac death.

Detection of a major risk factor for sudden death in an otherwise asymptomatic person often raises major difficulties in management, particularly where the only treatment available is invasive, such as the implantable defibrillator. Recent guidelines have described the appropriate use of this technology, but often difficulty remains. This is particularly the case where the condition is newly recognised and its natural history not yet extensively described. A 63 year old man, whose condition was diagnosed as Brugada syndrome, in whom this problem is illustrated is described.

Risk stratification in unstable angina and non-Q wave myocardial infarction using soluble cell adhesion molecules.

OBJECTIVE: To assess prospectively the prognostic value of soluble cellular adhesion molecules (CAMs) in patients with unstable angina and non-Q wave myocardial infarction and to compare their prognostic accuracy with that of C reactive protein (CRP). DESIGN AND SETTING: Prospective observational study of patients presenting acutely with unstable angina and non-Q wave myocardial infarction to a single south Dublin hospital. METHODS: Patients with Braunwald IIIA unstable angina and non-Q wave myocardial infarction had serum samples taken at presentation before initiation of antithrombotic treatment and were followed for six months. The primary end point was the occurrence of major adverse cardiovascular events (recurrent unstable angina, non-fatal myocardial infarction, and cardiovascular death) at six months. Concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble endothelial selectin, and soluble platelet selectin were measured using an enzyme linked immunosorbent assay technique. CRP was measured with an immunophelometric assay. RESULTS: 91 patients (73 men and 18 women, mean (SD) age 61 (11) years) were studied; 27 patients (30%) had major adverse cardiac events during the six months of follow up. Concentration of CRP were significantly raised in patients who had an ischaemic event (mean (SEM) 11.5 (6.4) mg/l v 5.4 (2.5) mg/l, p < 0.001). Concentrations of sVCAM-1 were also significantly raised in the ischaemic event group (979 (30) ng/ml v 729 (22) ng/ml, p < 0.001). Both sVCAM-1 and CRP concentrations correlated strongly with the occurrence of an adverse event. The sensitivity of CRP > 3 mg/l and sVCAM-1 > 780 ng/ml for predicting future events was > 90%. There was no difference in concentrations of sICAM-1, soluble endothelin selectin, or soluble platelet selectin between event and non-event groups. CONCLUSION: Raised concentrations of sVCAM-1 and CRP are predictive of an increased risk of major adverse cardiovascular events six months after presentation with unstable angina and non-Q wave myocardial infarction. These findings suggest that the intensity of the vascular inflammatory process at the time of presentation is a determinant of clinical outcome in unstable coronary artery disease.

Relationship between intracoronary and peripheral expression of soluble cell adhesion molecules.

BACKGROUND: Elevated levels of soluble cell adhesion molecules (sCAMs) have been reported in various coronary artery disease processes. The principle stimulus for expression of sCAMs is believed to be an inflamed atherosclerotic plaque within the coronary vessel. The relationship between levels of sCAMs in the coronary circulation and the peripheral circulation has not been defined. The primary aim of this study was to define the relationship between levels of sCAMs sampled from the systemic circulation and from the coronary circulation. We also set out to document the acute expression of soluble CAMs following coronary angioplasty with or without stent implantation. METHODS: The coronary sinus was cannulated in patients undergoing LAD angioplasty. Samples were drawn from left coronary ostium (LCO) and coronary sinus (CS) and femoral vein simultaneously before, immediately after and 4 h after the PTCA procedure. Levels of sICAM-1, sVCAM-1, sE-selectin and sP-selectin were measured using ELISA technique. RESULTS: 10 patients (7 male/3 female, 61+/-11 y) entered the study. There was no significant difference in the levels of sICAM-1, sVCAM-1, sE-selectin and sPselectin whether sampled from left coronary ostium, coronary sinus or femoral vein at all time points. There was no significant change in the acute expression of sICAM-1, sVCAM-1 and sE-selectin following coronary angioplasty. Levels of sP-selectin fell significantly during the PTCA procedure (142+/-7 ng/ml to 64+/-6 ng/ml, P<0.001) but then rose again after 4 h and returned toward baseline levels at 24 h. CONCLUSION: Levels of soluble CAMs sampled in the systemic circulation directly reflect levels in the coronary circulation. Coronary angioplasty results in rapid fall in levels of sP-selectin which returns to normal within 24 h following the procedure.

Impact of preexisting statin use on adhesion molecule expression in patients presenting with acute coronary syndromes.

Of 147 patients admitted with acute coronary syndromes, 17 were taking statins at the time of presentation. These were matched with 17 subjects not taking statins. We found that statin therapy was associated with lower levels of sP-selectin, a marker of platelet and vascular endothelial activation. This provides further insight into the extralipid effect of statins in clinical practice and may help explain the greater-than-expected benefits of statin therapy in ischemic heart disease.

Enhanced endothelial activation in diabetic patients with unstable angina and non-Q-wave myocardial infarction.

AIMS: Diabetes mellitus (DM) is associated with chronic endothelial dysfunction. Diabetic patients presenting with acute coronary syndromes have a worse prognosis than non-diabetics. An acute inflammatory reaction at the site of coronary plaque rupture and increased expression of surface and soluble cellular adhesion molecules (CAMs) are pathological features of acute coronary syndromes. We set out to characterize the expression of soluble CAMs in patients with and without diabetes presenting with unstable angina (UA) and non Q-wave myocardial infarction (NQMI). METHODS: Patients presenting with UA and NQMI had serum samples taken on presentation, after 72 h and then 3, 6 and 12 months after discharge. Levels of soluble intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin and P-selectin were measured using an ELISA technique. RESULTS: We studied 15 diabetic patients and 15 age- and sex-matched non-diabetic patients presenting with either UA or NQMI. Levels of soluble E-selectin were elevated in the diabetic patients in comparison with the non-diabetic patients at all measured time points: 74 +/- 10 ng/ml vs. 47 +/- 3 ng/ml, P < 0.03 at t = 0 h, 55 +/- 5 ng/ml vs. 38 +/- 2 ng/ml, P < 0.02 at t = 72 h. However, levels of soluble P-selectin were lower in the diabetic cohort during follow-up: 134 +/- 15 ng/ml vs. 225 +/- 32 ng/ml, P < 0.02 at t = 3/12 and 112 +/- 8 ng/ml vs. 197 +/- 23 ng/ml, P < 0.02 at t = 6/12. There was no significant difference in levels of soluble ICAM-1 and VCAM-1 between diabetic and non-diabetic patients. CONCLUSIONS: Levels of soluble E-selectin are significantly elevated in diabetic patients presenting with UA and NQMI in comparison with non-diabetics. This finding may reflect enhanced endothelial activation which may contribute to the adverse prognosis of diabetic patients with acute coronary syndromes.

Evidence of prolonged inflammation in unstable angina and non-Q wave myocardial infarction.

OBJECTIVES: This study was designed to document the inflammatory response up to one year after acute presentation with unstable angina (UA) and non-Q wave infarction (NQMI) as reflected by the expression of soluble cell adhesion molecules (CAMs). BACKGROUND: Coronary plaque inflammation is a key component in the pathogenesis of acute coronary syndromes. Cell adhesion molecules are critical mediators of the inflammatory process. Soluble forms of these molecules are detectable in serum and are elevated acutely in patients with UA and NQMI. METHODS: Patients presenting with UA and NQMI had serum samples taken at presentation and then after three, six and 12 months. A control group of similar age and gender distribution was used for comparison. Levels of soluble inter-cellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial-selectin and platelet-selectin were measured using an ELISA technique. RESULTS: We studied 91 patients (M/F = 73/18, mean age 62 +/- 11 years, 56 UA and 35 NQMI) and 24 controls (M/F = 18/6, mean age 56 +/- 12 years). Levels of all four soluble CAMs were significantly elevated in both UA and NQMI patients at presentation, three and six months in comparison with controls. Levels in UA and NQMI groups fell between six and 12 months after initial presentation. CONCLUSIONS: The results suggest that the inflammatory stimulus triggering expression of CAMs is sustained for up to six months after presentation with either UA or NQMI and then returns toward control values over the following six months.

Helicobacter pylori serology in patients with angiographically documented coronary artery disease.

We studied the relation between angiographically defined coronary artery disease and serologic evidence of Helicobacter pylori infection in 488 patients undergo ing elective coronary angiography. There was no association between Helicobacter pylori infection and coronary artery disease (odds ratio 1.3, 95% confidence interval 0.83 to 2.16).

Percutaneous catheter and guidewire fragmentation with local administration of recombinant tissue plasminogen activator as a treatment for massive pulmonary embolism.

The purpose of this article is to report four patients with massive pulmonary embolism treated with percutaneous catheter and guidewire fragmentation and local administration of recombinant tissue plasminogen activator (r-TPA). Four patients with massive pulmonary embolism initially underwent pulmonary angiography. Thrombus fragmentation was performed with both standard angiographic guidewires and catheters followed by local infusion of 41-200 mg of r-TPA. Pulmonary angiography was repeated after treatment. All patients survived with improvement in their clinical status and eventual discharge from hospital. Angiography in all patients post treatment demonstrated improvement in pulmonary perfusion (mean Miller score before treatment 22.5; mean Miller score after treatment 5.75). No patient had a significant complication. Mechanical fragmentation of the thrombus followed by local infusion of r-TPA was an effective treatment for massive pulmonary embolism in these four patients with no significant complications.