Chest pain unit management of patients at low and not low-risk for coronary artery disease in the emergency department. A 5-year experience in the Florence area.

In this study, we screened a total of 6723 consecutive patients with chest pain and ECG non-diagnostic for acute myocardial infarction (AMI) on presentation to the emergency department (ED). The aim of the study was to avoid missed AMI, improve safe early discharge and reduce inappropriate coronary care unit (CCU) admission. Chest pain patients were triaged using a clinical chest pain score and managed in a chest pain unit (CPU). Patients with a low clinical chest pain score were considered at very 'low-risk' for cardiovascular events and discharged from the ED; patients with a high chest pain score were submitted to CPU management. Observation and titration of serum markers of myocardial injury were obtained up to 6 hours. Rest or stress myocardial scintigraphy (SPECT) was performed in patients > 40 years or with > or = 2 major coronary risk factors. Exercise Tolerance Test (ETT) or Stress-Echocardiogram (stress-Echo) were performed in younger patients or with < 2 coronary risk factor, or unable to exercise, respectively We discharged directly from the ED the majority of patients (4454; 66%): in this group there was only a 0.2% final diagnosis of coronary artery disease (CAD) at follow-up. The remaining 34% of patients, with non-diagnostic or normal ECG, were managed in the CPU. In this group, 1487 patients (representing 22% of the overall study group) were found positive for CAD, two-thirds because of delayed ECG or serum markers of myocardial injury, and one-third by Echo, SPECT or ETT. In conclusion, CPU based management allowed 22% early detection of myocardial ischaemia and 78% early discharge from the ED avoiding inappropriate CCU admission and optimizing the use of urgent angiography.

Prospective evaluation of adenosine-induced proarrhythmia in the emergency room.

The arrhythmogenic hazard of adenosine treatment in an emergency room (ER) has not been established. Thus, in this study, we set out to prospectively determine the prevalence and clinical consequences of the arrhythmogenic effects associated with urgent adenosine treatment in the ER. One hundred and sixty consecutive patients treated with adenosine for regular wide or narrow complex tachyarrhythmias at our ER were included in the study. An initial bolus of 3 mg of adenosine was used, up to a maximum dose of 18 mg (mode 6 mg). Proarrhythmia was defined as the new appearance of any brady- or tachyarrhythmia within 1 minute from the bolus administration of adenosine. Of the 160 study patients, 84% had narrow complex tachycardia and 16% had wide complex tachycardia. Adenosine was effective in the diagnosis and/or treatment of the underlying arrhythmia in 92%. The overall prevalence of adenosine-induced proarrhythmia was 13%, including prolonged AV block inducing asystole > 4 seconds (7%), paroxysmal atrial fibrillation (1%) and non-sustained ventricular tachycardia (5%). All adenosine-induced arrhythmias were transient and subsided spontaneously. It is concluded, firstly, that adenosine-induced proarrhythmia proved to be frequent in a consecutive ER series, and included potentially dangerous arrhythmias. Secondly, nevertheless, all adenosine-induced arrhythmias subsided spontaneously and did not require treatment. Therefore, urgent adenosine treatment is safe and can be recommended in an emergency setting, provided a strict protocol of administration under close monitoring by highly trained personnel.

Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction.

BACKGROUND: The role of echocardiographic right ventricular (RV) dysfunction in predicting clinical outcome in clinically stable patients with pulmonary embolism (PE) is undefined. In this study, we assessed the prevalence and clinical outcome of normotensive patients with RV dysfunction among a broad spectrum of PE patients. METHODS AND RESULTS: This prospective clinical outcome study included cohort of 209 consecutive patients (age, 65+/-15 years) with documented PE. Acute RV dysfunction was diagnosed in the presence of >/=1 of the following: RV dilatation (without hypertrophy), paradox septal systolic motion, and Doppler evidence of pulmonary hypertension. Four groups were identified: 28 patients presenting with shock or cardiac arrest (13%), 19 hypotensive patients without shock (9%), 65 normotensive patients with echocardiographic RV dysfunction (31%), and 97 normotensive patients without RV dysfunction (47%). Among normotensive patients with RV dysfunction, 6 (10%) developed PE-related shock after admission: 3 of these patients died, and 3 were successfully treated with thrombolytic agents. In comparison, none of the 97 normotensive patients without RV dysfunction developed shock or died as a result of PE. CONCLUSIONS: A significant proportion (31%) of normotensive patients with acute PE presents with RV dysfunction; these patients with latent hemodynamic impairment have a 10% rate of PE-related shock and 5% in-hospital mortality and may require aggressive therapeutic strategies. Conversely, normotensive patients without echocardiographic RV dysfunction have a benign short-term prognosis. Thus, early detection of echocardiographic RV dysfunction is of major importance in the risk stratification of normotensive patients with acute PE.

Utility of an integrated clinical, echocardiographic, and venous ultrasonographic approach for triage of patients with suspected pulmonary embolism.

The potential role of ultrasound techniques in diagnosing acute pulmonary embolism (PE) has been investigated in severe cases with hemodynamic compromise, but is still unclear for the whole clinical spectrum of patients with suspected PE. The aim of this study was to assess the utility of an integrated bedside evaluation for PE based on the combination of a clinical score, 2-dimensional echocardiography, and color venous duplex scanning. A group of 117 consecutive patients with suspected PE was assessed using a clinical likelihood score, echocardiography, and venous duplex scanning in order to obtain a preliminary diagnosis of PE, which was subsequently compared with the final diagnosis obtained by lung perfusion scintigraphy and angiography. A preliminary diagnosis of PE was made in 70 patients; a final diagnosis of PE was made in 63 patients, of which 56 had and 7 did not have a preliminary diagnosis of PE. The preliminary diagnosis therefore showed 89% sensitivity and 74% specificity, with a total accuracy of 82%. In patients with massive PE, sensitivity and negative predictive values of the preliminary diagnosis were 97% and 98%, respectively. Echocardiography was poorly sensitive (51%) but highly specific (87%) for PE. Thus, the integration of clinical likelihood, echocardiography, and venous duplex scanning provides a practical approach to patients with suspected PE, allows the rapid implementation of appropriate management strategies, and may reduce or postpone the need for further instrumental evaluation of more limited access.

Efficacy and safety of adenosine in diagnosis and treatment of regular tachycardia in the elderly.

BACKGROUND: Adenosine is currently used in the treatment and differential diagnosis of regular tachycardia. However, the efficacy of its employment has not been studied in elderly people. METHODS: We evaluated the safety, and the diagnostic and therapeutic utility of adenosine in elderly people aged over 70 years with regular sustained tachycardia, compared with a group of patients aged under 70 years affected by the same arrhythmia. Adenosine was given to 107 patients in increasing bolus doses up to 18 mg during regular broad and narrow complex tachycardia; 49 patients were aged 70 and over, and 58 patients were aged less than 70 years. In the former group, surface ECG showed 38 narrow complex tachycardias and 11 broad complex ones; in the second group there were 48 narrow complex tachycardias and 10 broad complex ones. RESULTS: Adenosine was effective in 94% of the elderly patients and in 93% of the younger patients. In the group aged over 70 years, adenosine restored sinus rhythm in 37% of patients and revealed the mechanism of arrhythmia in 57%. Adenosine restored sinus rhythm in 50% of patients under 70 years and revealed atrial or sinus tachycardia in 43%. The incidence of symptomatic side effects and peri-conversion ventricular arrhythmias was similar in the two groups. There were ventricular pauses over 3 s long in four (8%) of the older patients (maximum pause 7 s) and in two patients (3%) of the group under 70 years (maximum pause 6 s). No adverse haemodynamic effects were observed. CONCLUSION: These data demonstrate the safety and the value of adenosine in the diagnosis and treatment of regular tachycardia in elderly patients.

Excessive vasoconstriction after stress by the aging kidney: inadequate prostaglandin modulation of increased endothelin activity.

The adaptive capacity of the aging kidney to stimulation of the sympathetic nervous system, as induced by a 30-minute mental stress (MS), was assessed in 8 elderly healthy women (68 to 82 years of age) and compared with that of 8 younger women (24 to 40 years of age). The study encompassed 4 consecutive 30-minute periods (baseline, mental stress, recovery 1, and recovery 2). In the elderly subjects, baseline effective renal plasma flow (ERPF)(iodine 131-labeled hippurate clearance) was lower and glomerular filtration rate (GFR)(iodine 125-labeled iothalamate clearance) was proportionally less reduced than in the younger group; the filtration fraction (FF) was higher. The elderly group excreted more endothelin 1 (ET-1) (P < .05), prostaglandin E2 (PGE2), and 6-keto-prostaglandin F1alpha (6-keto PGF1alpha)(P < .001 for both)(radioimmunoassay). Mental stress induced similar increases in blood pressure, heart rate, and plasma catecholamines in the 2 age groups, limited to the stimulation period. In the elderly group, mental stress caused a prolonged decrease in ERPF that reached its maximum 60 minutes after mental stress (-33%, P < .05), while GFR remained constant during the whole experiment, so that FF increased. In the younger subjects, renal hemodynamic changes were limited to the mental stress period. ET-1 increased during mental stress and the first recovery period in the elderly group (+50% and +25%, P < .05) as it did in the younger group, but the elderly group differed from the younger in that vasodilating prostaglandins increased only during mental stress. In conclusion, the aging kidney reacts to adrenergic stimulation with more-pronounced and -prolonged vasoconstriction that is probably caused by a defect in prostaglandin modulation of endothelin activity. Autoregulation of GFR is maintained at the expense of increased intraglomerular pressure.

Renal adaptation to stress: a possible role of endothelin release and prostaglandin modulation in the human subject.

The aim of this study was to define the neurohumoral response associated with the renal hemodynamic perturbations induced by mental stress acting as an adrenergic stimulus. In 8 healthy women, the effects of mental stress were studied during four consecutive 30-minute periods (baseline, mental stress, recovery I, recovery II). Mental stress induced sympathetic activation as evidenced by increases in blood pressure, heart rate, and plasma norepinephrine level. Effective renal plasma flow (iodine 131-labeled hippurate clearance) decreased only during mental stress (-22%, p < 0.05 vs baseline); glomerular filtration rate (iodine 125-labeled iotalamate clearance) remained constant during the entire experiment; the filtration fraction increased significantly during mental stress and recovery I (+30% and +22%, respectively, p < 0.02 for both). Complex neuroendocrine responses were associated with the hemodynamic changes. Urinary excretion of endothelin-1 and 6-keto-PGF(1alpha) increased during mental stress (+53%, p < 0.01, and +20%, p < 0.01, respectively) and recovery I (+49% and +29%, respectively, p < 0.01 for both). Urinary cyclic guanosine monophosphate rose only during mental stress (+77%, p < 0.05), whereas excretion of PGE2 showed a stepwise increase throughout recovery I and II (+292%, p < 0.01, and +360%, p < 0.001, respectively). In conclusion, the present experiments demonstrate that renal hemodynamic response induced by mental stress is a complex reaction in which endothelin-1, prostaglandins, and presumably nitric oxide take part.

Venous dural sinus thrombosis in a middle-aged woman with anticardiolipin antibodies.

Anticardiolipin antibodies are circulating autoantibodies directed against phospholipids. They have been previously associated with systemic venous and arterial but not with cerebral venous thrombosis. We describe the case of a middle aged woman with circulating anticardiolipin antibodies who suffered from dural sinus transversus and jugular venous thrombosis documented by Nuclear Magnetic Resonance (NMR).

[Acute pulmonary edema and a state of shock in a female patient with a penbutolol-treated pheochromocytoma]. / Edema polmonare acuto e stato di shock in una paziente affetta da feocromocitoma trattata con penbutololo.

A woman with "mild arterial hypertension" had a cardiogenic shock a few minutes after taking the first tablet of penbutolol. Subsequently, a suprarenal pheochromocytoma was discovered (and surgically excised, with stable recovery).

[Acute renal failure caused by treatment with diuretics and ACE inhibitors in the absence of renal artery stenosis]. / Insufficienza renale acuta da trattamento con diuretici ed ACE inibitori in assenza di stenosi delle arterie renali.

The Authors describe a clinical case of a patient affected by arterial hypertension of severe degree (IV grade OMS) that during therapy with ACE inhibitors and diuretics developed acute renal failure that reversed after stopping treatment. The clinical course was quite similar to acute renal failure induced by ACE inhibitors and diuretics in patient with bilateral renal artery stenosis. In interpreting the pathogenesis, the Authors suppose, beside a reductions of effective plasma flow, the coexistence of hyalinosis of renal arterioles. They underline the necessity of monitoring renal function at least in the first weeks of therapy when a treatment with ACE inhibitors and diuretics is started especially in patients with hypertension of high degree and/or reduced renal function.

The renal excretory activity of atrial natriuretic factor is independent of renal prostaglandins in humans.

Since renal prostaglandins may contribute to natriuresis induced by endogenous atrial natriuretic factor (ANF), acute volume expansion (AVL), a known stimulus of ANF and prostaglandins, was induced in 8 healthy women in order to test whether the consequent sodium and water diuresis is altered by prostaglandin inhibition. AVL (i.v. infusion of a 2 liter 5% glucose solution in 1 h) was infused after placebo and after inhibition of prostaglandins with diclofenac (200 mg/day orally for 4 days), in a double blind randomized cross-over fashion. Urinary eicosanoids (PGE2, PGF2 alpha, 6-ketoPGF1 alpha, TXB2--RIA), plasma ANF (RIA) and urinary electrolytes were determined before, during and after AVL under both placebo and diclofenac regimes. During placebo, AVL induced sustained increases in plasma ANF (174% at peak, p less than 0.001 ANOVA), excretion of the four eicosanoids (149%-1172%, p less than 0.005-0.001), urinary volume (UV, 815%, p less than 0.001), natriuresis (UNa, 98%, p less than 0.005) and in kaliuresis (UK, 90%, p less than 0.001). Cyclooxygenase inhibition resulted in a reduction of over 70% in both baseline values and AVL-induced increase of eicosanoids. It did not alter either baseline levels or AVL-stimulated ANF, UV, UNa and UK in relation to placebo. The present results suggest that the diuretic and natriuretic activity of ANF is not mediated by renal PGs in humans.