Role of the ECG in initial acute coronary syndrome triage: primary PCI regardless presence of ST elevation or of non-ST elevation.

The major initial triaging decision in acute coronary syndrome (ACS) is whether or not percutaneous coronary intervention (PCI) is the primary treatment. Current guidelines recommend primary PCI in ST-elevation ACS (STEACS) and initial antithrombotic therapy in non-ST-elevation ACS (NSTEACS). This review probes the question whether this decision can indeed be based on the ECG. Genesis of STE/NSTE ECGs depends on the coronary anatomy, collateral circulation and site of the culprit lesion. Other causes than ischaemia may also result in ST-segment changes. It has been demonstrated that the area at risk cannot reliably be estimated by the magnitude of the ST change, that complete as well as incomplete occlusions can cause STE as well as NSTE ECGs, and that STE and NSTE patterns cannot differentiate between transmural and non-transmural ischaemia. Furthermore, unstable angina can occur with STE and NSTE ECGs. We conclude that the ECG can be used to assist in detecting ischaemia, but that electrocardiographic STE and NSTE patterns are not uniquely related to distinctly different pathophysiological mechanisms. Hence, in ACS, primary PCI might be considered regardless of the nature of the ST deviation, and it should be done with the shortest possible delay, because 'time is muscle'.

Left atrial appendage occlusion in recurrent ischaemic stroke, a multicentre experience.

BACKGROUND: Oral anticoagulation therapy (OAC) remains the gold standard for ischaemic stroke prevention in patients with non-valvular atrial fibrillation (NVAF) and elevated stroke risk. Percutaneous left atrial appendage occlusion (LAAO) has emerged as a potential alternative for stroke prevention in patients who cannot tolerate OAC. Although no randomized data is available, recurrent stroke in NVAF-patients, while on adequate OAC, is regarded as a treatment failure and therefore is considered as a potential indication for LAAO, based upon expert opinion. METHODS/OBJECTIVES: A multicentre retrospective cohort study evaluating efficacy, safety and mortality of LAAO in NVAF-patients presenting with recurrent ischaemic stroke, after excluding other plausible causes. RESULTS: Fifteen LAAO have been performed in NVAF-patients with recurrent stroke despite ongoing OAC, after exclusion of other plausible causes. Mean age was 78.1 ± 5.8 years, mean CHA2DS2-VASc-score = 6 ± 1.2 and mean HAS-BLED-score = 5 ± 1.2. Successful implantation was achieved in all patients (73% Amplatzer device and 27% Watchman device), without any access-related complications and only one procedure/device-related complication (device embolization) was reported. In all but four patients, OAC was continued at long term after LAAO. No haemorrhagic strokes and only two ischaemic strokes were observed. During follow-up three patients died, all due to non-atrial fibrillation or non-device-related causes. CONCLUSIONS: In NVAF-patients at high risk for stroke presenting with recurrent stroke despite adequate OAC, LAAO may be considered an adjunctive, but not alternative treatment to OAC with high feasibility and safety.Abbreviations: AF: atrial fibrillation; ESC: European Society of Cardiology; INR: international normalized ratio; LAA: left atrial appendage; LAAO: left atrial appendage occlusion; NOAC: non-vitamin K oral anticoagulants; NVAF: non-valvular atrial fibrillation; OAC: oral anticoagulation; RS: recurrent (ischaemic) stroke; SD: standard deviation; TIA: transient ischaemic attack; TOE: transoesophageal echocardiography; TTE: transthoracic echocardiography; VKA: vitamin K antagonists.

Air pollution and ST-elevation myocardial infarction: A case-crossover study of the Belgian STEMI registry 2009-2013.

BACKGROUND: Previous studies have shown that air pollution particulate matter (PM) is associated with an increased risk for myocardial infarction. The effects of air pollution on the risk of ST-elevation myocardial infarction (STEMI), in particular the role of gaseous air pollutants such as NO2 and O3 and the susceptibility of specific populations, are still under debate. METHODS: All patients entered in the Belgian prospective STEMI registry between 2009 and 2013 were included. Based on a validated spatial interpolation model from the Belgian Environment Agency, a national index was used to address the background level of air pollution exposure of Belgian population. A time-stratified and temperature-matched case-crossover analysis of the risk of STEMI was performed. RESULTS: A total of 11,428 STEMI patients were included in the study. Each 10µg/m3 increase in PM10, PM2.5 and NO2 was associated with an increased odds ratio (ORs) of STEMI of 1.026 (CI 95%: 1.005-1.048), 1.028 (CI 95%: 1.003-1.054) and 1.051 (CI 95%: 1.018-1.084), respectively. No effect of O3 was found. STEMI was associated with PM10 exposure in patients ≥75y.o. (OR: 1.046, CI 95%: 1.002-1.092) and with NO2 in patients ≤54y.o. (OR: 1.071, CI 95%: 1.010-1.136). No effect of air pollution on cardiac arrest or in-hospital STEMI mortality was found. CONCLUSION: PM2.5 and NO2 exposures incrementally increase the risk of STEMI. The risk related to PM appears to be greater in the elderly, while younger patients appear to be more susceptible to NO2 exposure.

Comparison of transthoracic echocardiography with second harmonic imaging with transesophageal echocardiography in the detection of right to left shunts.

We compared the use of transthoracic echocardiography with second harmonic imaging after a peripheral intravenous injection of an agitated saline solution with transesophageal echocardiography (TEE) in the detection of right to left shunts at the cardiac and pulmonary level. Second harmonic mode transthoracic echocardiography and TEE are equally sensitive in detecting right to left shunts in patients undergoing a daily routine TEE.

Identification of a D1 dopamine receptor, not linked to adenylate cyclase, on lactotroph cells.

1. We studied the lactotroph cells of the rat by both in vivo and in vitro pharmacological techniques for the presence of D1-receptors. Both approaches revealed the presence of D2-receptor, stimulated by quinpirole (resulting in an inhibition of prolactin secretion) and blocked by domperidone. 2. Administration of fenoldopam, the most selective D1-receptor agonist currently available, resulted in a dose-dependent decrease of prolactin secretion in vivo (after pretreatment with alpha-methyl-p-tyrosine) and in vitro (cultured pituitary cells). This increase was dose-dependently blocked by the selective D1-receptor antagonist, SCH 23390, and although the effect of fenoldopam was less than that obtained by D2-receptor stimulation, these data suggest that a D1-receptor also controls prolactin secretion. 3. In order to detect the location of these dopamine receptors, autoradiographic studies were performed by use of [3H]-SCH 23390 and [3H]-spiperone as markers for D1- and D2-receptors, respectively. Specific binding sites for [3H]-SCH 23390 were demonstrated. Fenoldopam dose-dependently reduced [3H]-SCH 23390 binding, but had no effect on [3H]-spiperone binding. Immunocytochemical labelling of prolactin cells after incubation with [3H]-SCH 23390 revealed that the granulae and hence, D1 binding sites were present on the lactotroph cells. 4. Radioligand binding studies performed on membranes from anterior pituitary cells revealed the presence of the D2-receptor (54 fmol mg-1 protein) with a Kd of 0.58 nM for [3H]-spiperone, but failed to detect D1-receptors. 5. Finally, we studied the effect of dopamine and of fenoldopam on the adenosine 3':5'-cyclic monophosphate (cyclic AMP) content of anterior pituitary cells. Although cyclic AMP increased upon prostacyclin administration, indicating an intact adenylate cyclase system, fenoldopam failed to increase the cyclic AMP production. 6. It is tempting to speculate that fenoldopam reduces prolactin secretion through interaction with a non-cyclase-linked D1-receptor on the lactotroph cells.

Increased dopamine-induced nephrogenous cAMP formation in hypertension.

Low doses of exogenous dopamine (3 micrograms/kg/min) were administered intravenously to nine patients with essential hypertension and to six age-matched healthy volunteers. During infusion with dopamine, mean arterial blood pressure decreased in hypertensive patients whereas it did not change in normotensive subjects. Basal levels of sodium excretion were comparable in hypertensive and normotensive subjects. The natriuretic response to dopamine was significantly greater in hypertensive patients. Urinary and nephrogenous cAMP significantly increased in both normotensive and hypertensive subjects. The increase of nephrogenous cAMP was more pronounced in hypertensive patients than in normotensive controls. A significant correlation was found between nephrogenous cAMP and sodium excretion. The enhanced natriuretic response to dopamine in hypertensive patients may be due to increased cAMP formation in response to tubular dopamine receptor stimulation. This is in agreement with the hypothesis of either up-regulation or affinity changes of renal dopamine receptors in patients with essential hypertension, secondary to a decreased endogenous production of intrarenal dopamine.

Effects of fenoldopam on alpha-methyl-p-tyrosine-stimulated prolactin secretion in conscious rats.

Pituitary dopamine D-2 receptors participate in the regulation of prolactin (PRL) release. No dopamine D-1 receptors have so far been identified in the pituitary gland. The present study was designed to assess the effects of fenoldopam, a selective dopamine D-1 receptor agonist, on alpha-methyl-p-tyrosine-stimulated PRL release. Fenoldopam dose dependently reduced the alpha-methyl-p-tyrosine-stimulated PRL secretion. This inhibitory effect of fenoldopam was abolished after pretreatment with SCH 23390, a specific dopamine D-1 receptor antagonist, suggesting the involvement of a dopamine D-1 receptor in PRL secretion.

Tricuspid stenosis: a rare complication of pacemaker-related endocarditis.

We report a case of recurrent pacemaker lead endocarditis as the cause of acquired tricuspid stenosis. The diagnosis was made noninvasively by 2-dimensional Doppler echocardiography. The case was further complicated by a paradoxical septic embolism through a patent foramen ovale. This cascade of rear events after a pacemaker implantation has never been described in the literature before.

Pulmonary stenosis caused by extrinsic compression of an aortic pseudoaneurysm of a composite aortic graft.

Pulmonic stenosis and stenosis of the right ventricular outflow tract related to extrinsic compression have been described in patients with tumors, in a patient with a pericardial cyst, and in patients with vascular abnormalities as an unruptured sinus of Valsalva aneurysm, a giant coronary artery pseudoaneurysm and an aortic arch aneurysm. Composite graft replacement of the ascending aorta and aortic valve with reimplantation of the coronary arteries has some inherent complications. Our case report describes a patient with a pericomposite graft aneurysm presenting as a stenosis of the pulmonary artery, detected by Doppler echocardiography.

Antihypertensive efficacy of low dose torasemide in essential hypertension: a placebo-controlled study.

The blood pressure lowering effect of chronic treatment with the low, non-diuretic dose of 2.5 mg of torasemide, a new loop-diuretic, was assessed in 20 patients with mild to moderate essential hypertension (WHO stage I-II) in a randomised, double-blind, balanced, placebo-controlled, cross-over study. Blood pressure was significantly reduced after four weeks of torasemide as compared to four weeks of placebo. No significant diuretic effect was detected and there were no relevant metabolic or clinical side effects. The present results show that torasemide 2.5 mg once daily has a significant BP lowering effect and is well tolerated in patients with mild to moderate hypertension. This low dose, lacking significant diuretic activity, appears to be the recommended dose for starting antihypertensive treatment with this compound.

Quantitative assessment of regional dysfunction from gated single photon emission tomography myocardial perfusion studies: a non-segmental approach.

We present a modified (non-segmental) method for quantification of regional left ventricular dysfunction using gated myocardial perfusion SPET. Gated SPET is increasingly used to obtain complementary information on local perfusion and to assess the relevance of deficits in segmental count densities (attenuation vs perfusion deficit). The non-segmental approach was motivated by a hypothetical limitation regarding the validity of commonly used methods of quantitative wall thickening (WT) analysis. These methods are all based on segmental analysis, which could cause underestimation of 'true' contractile dysfunction in perfusion defects that do not have a strict segmental distribution. SPET images gated in eight time bins 60 min after the injection of 740 MBq 99Tcm-tetrofosmin or 99Tcm-sestamibi were recorded on a triple-headed camera in 20 normal subjects and in 16 patients within 2 weeks and again 3 months after myocardial infarction. Normal limits of wall thickening, calculated from pooled wall thickening profiles obtained in normal subjects, were used to identify and quantify areas with abnormal wall thickening in patients with coronary artery disease. The method was validated against data obtained from contrast ventriculography (CVG) and tested for reproducibility. The reproducibility of the method was excellent: r = 0.98 (WTsev measure 1 = 1.03WTsev measure 2 - 0.01). The localization of wall thickening abnormalities detected by gated SPET correlated well with the localization of regions with abnormal wall motion (WM) identified by CVG. The severity of the regional myocardial dysfunction assessed by gated SPET was closely correlated with the severity of the regional myocardial dysfunction derived from CVG: r = 0.85 (WMsev = 2.55WTsev + 2.30). Furthermore, a good correlation between the total wall thickening severity score and the global left ventricular ejection fraction (LVEF) was observed early and late after myocardial infarction: r = 0.80 (WTsev = -0.4LVEF + 0.46). We conclude that quantitative analysis of regional wall thickening assessed from gated SPET myocardial perfusion scintigraphy is a reliable parameter for regional ventricular function. Categorizing wall thickening abnormalities quantitatively may be helpful in assessing small changes in regional function that may occur between sequential gated SPET images.

Dipyridamole-induced angina pectoris during sestamibi stress test in patients with significant coronary artery disease: clinical, angiographic, and nuclear determinants.

Intravenous dipyridamole induces angina pectoris (AP) in some patients with significant coronary artery disease (CAD). The aim of this prospective study was to identify the angiographic, nuclear, and clinical determinants. The authors examined 50 patients consecutively with significant CAD on coronary angiography. All antiischemic medications were stopped twenty-four hours (nitrates only 6 hours) before injection of dipyridamole (0.84 mg/kg). ECGs were taken before, during, and after this injection. The regional myocardial activity of Tc-99m-Sestamibi at rest and after dipyridamole injection was measured with single-photon emission computed tomography (SPECT). During dipyridamole injection 20 patients had AP, of whom 15 had ST segment depression on ECG (P < 0.001). The only significant difference on coronary angiography between patients with dipyridamole-induced AP and those without AP was the presence of collaterals (P < 0.05). In patients with AP and collaterals, ECG and SPECT changes were always noted in the collateralized territory. Subgroup analysis showed that patients without previous myocardial infarction (MI, n = 17, P < 0.05) or nontransmural MI (n = 17, P < 0.05) had a good correlation between collaterals and AP, whereas patients with a history of transmural MI (n = 16) did not. No further significant variables could be found as a predictor of AP after dipyridamole injection. These findings suggest that AP during dipyridamole stress test is due to ischemia, which is not related to the severity of CAD. Ischemia is probably due to coronary steal to the collateralized territory in patients without transmural MI. Dipyridamole-induced angina pectoris is predictive for collaterals and may indicate viability in patients with MI.

Early electrocardiographic signs in acute massive pulmonary embolism.

As a result of the increasing accuracy in diagnosing acute pulmonary embolism by isotopic ventilation-perfusion scintigraphy and pulmonary arterial angiography, the electrocardiographic changes associated with acute cor pulmonale are being abandoned as a diagnostic tool for this life-threatening disease. Nevertheless, certain electrocardiographic findings can raise the suspicion of pulmonary embolism. In our view the electrocardiogram does have some merits in the emergency work-up of a patient with a high suspicion of pulmonary embolism. In this case report we emphasize the importance of the electrocardiographic findings which forwarded the diagnosis of pulmonary embolism. Hence the necessary invasive diagnostic and therapeutic measures, i.e. pulmonary arterial angiography and thrombolytic therapy, can be taken immediately after admission to the emergency department.

In vivo visualization of 111In labeled CD133+ peripheral blood stem cells after intracoronary administration in patients with chronic ischemic heart disease.

AIM: Stem cell homing to injured tissue is necessary for local tissue repair. But homing of stem cells in chronic ischemic heart disease (CIHD) is poorly understood. This study investigated homing of peripheral blood stem cells (PBSC) expressing the CD133 antigen. After intracoronary injection. The cells were (111)In labeled for in vivo visualization. METHODS: PBSC were mobilized with granulocyte-colony stimulating factor and collected by apheresis on d-1. On d0, CD133+ cells were enriched up to a median purity of 89% (range: 79-97%) with an immunomagnetic separation device (CliniMACS, Miltenyi). A fraction of the cells was radiolabeled with [(111)In]oxine in 0.1 M TRIS at pH 7.4 for 45-60 min. Cell viability after labeling was assessed using trypan-blue. The cells were injected at a radioactive concentration of 0.9 MBq/10(6) cells into the target open coronary vessel through a balloon catheter. During balloon inflation [(99m)Tc]sestamibi was injected intravenously to identify the myocardium and the target vascular territory. Eight patients (mean age: 53 years; range: 50-72 years) with stable CIHD and reduced left ventricular function (NYHA class I-II) after acute myocardial infarction (>12 months) were studied. After a first cohort of 3 patients received an injectate of 5-10 x 10(6) cells, our final protocol was applied in 5 patients in whom an average of 34.4 x 10(6) (range: 18.6-49.4) CD133+ cells was injected. Whole body and single photon emission computed tomography (SPECT) scans were acquired at different time points after injection (energy windows set at 140, 171 and 245 keV). Residual activity in the heart was assessed by drawing a region of interest around the heart on the anterior whole body views. RESULTS: Mean labeling efficiency of [111In]oxine labeling was 51.2% and cell viability after labeling averaged 88%. In the 5 patients receiving the higher amount of labeled cells, a clear (111)In-signal was observed in the heart region up to 3 days after administration. Fused [(99m)Tc]sestamibi/(111)In SPECT images demonstrated that the regional distribution of the transplanted cells within the target zone, as delineated by the flow tracer, remained unchanged over time. A biodistribution study in 2 patients showed a residual activity in the heart, liver and spleen of 6.9-8%, 23.1-26.8%, 3.1-3.7%, respectively, after 1-2 h and 2.3-3.2% 23.8-28.3%, 3.5-3.8%, respectively, after 12 h (decay corrected and expressed as a percentage of total body initial activity). No adverse events were observed during the procedure and up to 3 months follow-up. CONCLUSIONS: Radiolabeling with [(111)In]oxine is a suitable method for follow-up of cell distribution during the first days after transplantation. A significant amount of CD133+ PBSC home to the heart after intracoronary injection in patients with CIHD. The results of this study are useful for the design of trials that evaluate the tissue repair potential of CD133+ PBSC in the setting of CIHD.

Further studies on the mechanism of the natriuretic response to low-dose dopamine in man: effect on lithium clearance and nephrogenic cAMP formation.

The effect of intravenous infusion of low-dose dopamine on electrolyte excretion, lithium clearance, nephrogenous cAMP formation and renal haemodynamics was investigated in healthy volunteers. Dopamine significantly increased the urine flow rate by 70.6% and urinary sodium excretion by 72%, but did not change creatinine clearance, PRA or plasma levels of AVP, ANP and cAMP. Renal plasma flow significantly increased by 48.6%; the glomerular filtration rate was not changed. Lithium per se increased basal PRA, but had no effect on the increments of urine flow rate, sodium excretion and renal blood flow induced by dopamine. Dopamine significantly increased the fractional excretion of lithium (representing fractional excretion of sodium at the proximal level). The increase in urinary sodium excretion during dopamine infusion, significantly correlated with the increase in fractional excretion of lithium (r = 0.94; P less than 0.01) and the increase in nephrogenous cAMP formation (r = 0.96; P less than 0.01). No correlation was found between the increase in urinary sodium excretion and the increase in renal blood flow. In conclusion, this study confirms that low-dose dopamine increases renal blood flow and urinary sodium excretion in healthy volunteers. This natriuretic response appears to be due to interaction with proximal tubular dopamine receptors, which are positively coupled to adenylate cyclase.

The safety of adding carvedilol to hypertensive patients inadequately treated with diuretics.

A single-blind, single-center study was conducted to investigate the short-term safety and efficacy of carvedilol, a new cardiovascular agent, when added to 25 mg hydrochlorothiazide (HCTZ) as combination therapy for patients inadequately treated with HCTZ alone. A total of 18 patients entered the baseline study phase, during which they received 25 mg HCTZ once daily for 4 weeks; 16 of these patients (8 men and 8 women) entered the combination treatment phase. All patients had a supine diastolic blood pressure (DBP) of greater than or equal to 95 mm Hg prior to receiving the first dose of combination treatment. Combination treatment consisted of 25 mg HCTZ plus 12.5 mg carvedilol once daily for 2 days, followed by a forced titration of the carvedilol dose to 25 mg for 7 days. After 2 days of 12.5 mg carvedilol plus 25 mg HCTZ once daily, mean trough blood pressure was reduced as compared with baseline values. Of 16 patients, 6 (38%) achieved a trough supine DBP of less than 90 mm Hg. After 1 additional week of combination therapy with 25 mg carvedilol, 8 of 15 patients (53%) achieved a trough supine DBP of less than 90 mm Hg and 14 of 15 patients (93%) achieved that of less than 95 mm Hg. At each visit during the combination treatment phase, the acute reduction in blood pressure was greatest during the first 2 h after dosing. The heart rate was minimally affected by combination treatment with carvedilol at either trough levels or acutely after dosing. Nine patients experienced adverse events during combination treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Native valve endocarditis with aorta-to-left atrial fistula due to Corynebacterium amycolatum.

Infective endocarditis remains a pathology with a high rate of complications and mortality. One of the most dramatic complications is abscess formation. A rare evolution of abscess formation is the development of fistula. We describe an 88-year-old woman with an aortic root abscess and aorta-to-left atrial fistula. To our knowledge this has only been described with streptococcus species as causative micro-organism. In this case the abscess was caused by Corynebacterium amycolatum, which is an infrequently found micro-organism.