Emotional attitudes to AMI symptoms and inadequate coping strategies are the major determinants of patient decision delay. They should be considered as a key factor in patient and public education. Modification of these emotional factors might best be achieved by an individualized approach.

Apart from a higher frequency of severe dyspnea in diabetics, there appears to be no difference in the clinical symptoms of AMI patients with and without diabetes mellitus. AMI with little or no angina was also frequently found in non-diabetics. In the hospital, diabetics with suspected AMI do not appear to need a special judgement of symptoms. This could accelerate access of diabetics to standard therapeutic procedures.

Despite significant activation of the ANP system, reflected by a dose-dependent increase in plasma cyclic GMP concentrations, high doses of candoxatril induced systemic vasoconstrictory rather than vasocilatory effects in patients with CHF. Therefore NEP inhibition by candoxatril may not exhibit beneficial haemodynamic effects in CHF.

Urodilatin (ANF(95-126)) is an analogue of the atrial natriuretic factor (ANF(99-126)), which has been isolated from human urine. Recently we have shown in healthy volunteers, that intravenous bolus injections of synthetic urodilatin produce more pronounced reductions of pulmonary arterial pressure than ANF(99-126). To compare haemodynamic and renal effects of synthetic urodilatin with those of ANF(99-126) in congestive heart failure (CHF), 12 patients (66.3 +/- 1.4 years) received either two high dose intravenous bolus injections of 4 micrograms kg-1 bw Urodilatin (URO) at a 30 min interval (n = 6) or the same doses of ANF(99-126) (n = 6). Prior to i.v. URO, no URO immunoreactivity was found in human plasma (specific RIA, no crossreactivity to ANF). Similar to ANF, the increase in diuresis (1.4 +/- 0.7 to 3.7 +/- 1.6 ml min-1) and natriuresis (169 +/- 114 to 430 +/- 197 mumol min-1) was moderate after URO in CHF. During the 90 min study period, mean plasma cyclic GMP levels increased much more after URO (by 53.4 +/- 15.1 nM) than after ANF (by 13.1 +/- 3.0 nM; P = 0.04). In contrast to ANF, i.v. bolus injections of URO produced sustained haemodynamic effects in CHF lasting up to 90 min: The average (0-90 min) reduction of systemic vascular resistance was more pronounced after URO (-578 +/- 148) than after ANF (-204 +/- 65 dyn*s*cm-5, P = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Urodilatin (ANF(95-126)), an analogue of the atrial natriuretic factor (ANF(99-126)), has recently been isolated from human urine. To study haemodynamic and renal effects of synthetic urodilatin, 18 healthy male volunteers (age 26.1 +/- 0.8 years; X +/- SEM) received i.v. bolus injections of urodilatin at doses of 1, 2 or 4 micrograms kg-1 body weight (bw) (n = 6 per dosage group). Urodilatin dose-dependently increased heart rate and cardiac index. A dose-dependent increase in plasma cyclic GMP levels was also observed. Urinary cyclic GMP excretion, urine flow and natriuresis increased 7-fold, 5-fold and 4-fold, respectively. Renal effects were not different between dosage groups. Compared with ANF(99-126), after urodilatin the reduction in mean pulmonary arterial pressure (PAP) was more pronounced (2 micrograms kg-1, n = 6; ANF -1.8 +/- 0.5, URO: -5.5 +/- 1.1 mmHg, P less than 0.05). Furthermore, after urodilatin the reduction of PAP lasted continuously from 2 up to 90 min after injection, while ANF(99-126) produced only a transient decrease of PAP. Similarly the reduction of pulmonary capillary wedge pressure (PCWP) by urodilatin from 9.3 +/- 1.2 to 3.8 +/- 0.9 mmHg (P less than 0.05) was also sustained up to 90 min post administration. These data in healthy volunteers suggest that, due to prolonged reduction of PAP and PCWP with increases of cardiac index and reduction of systemic vascular resistance, urodilatin might exhibit beneficial effects in cardiovascular disease.

The effects of a continuous i.v. infusion of urodilatin at a dose of 30 ng kg-1 min-1 were studied in a patient with congestive heart failure. After 30 min, urodilatin had induced a marked stimulation of plasma cyclic GMP concentrations. In parallel haematocrit increased. No significant diuresis and no change of invasive haemodynamics was observed. After 2 h the patient developed a profuse perspiration. Eighty minutes later he suffered from dizziness due to hypotension (blood pressure 80/40 mmHg) and a sudden bradycardia (50 bpm). Urodilatin was discontinued and symptoms were relieved by bed tilt and rapid infusion of isotonic saline solution. Mechanisms contributing to these adverse effects may be fluid extravasation to the third space and sympathoinhibitory effects known to occur with natriuretic peptide infusion.

Moyamoya syndrome is characterized by the reticulated collateralization of the intracranial vasculature distal to an occlusion of proximal intracranial vessels. In the present study this pathology was visualized in 2 patients, aged 29 and 32 years, using transcranial color Doppler imaging (TCDI). Digital subtraction angiography in both patients revealed stenosis of the intracranial portion of the internal carotid arteries, occlusion and stenosis of several cerebral arteries, and a bilateral reticulated collateral network particularly in the region of both basal ganglia, typical of moyamoya syndrome. TCDI with power-mode Doppler depicted parts of the intracranial collateral network, not possible using conventional color-flow Doppler. TCDI with power-mode Doppler permitted better visualization of intracranial vascular pathology in comparison to conventional color-flow Doppler, enabling a rapid and noninvasive diagnosis of rare cerebrovascular anomalies.

Among patients presenting at the hospital with an acute myocardial infarction (AMI), about 2–6% are mistakenly discharged by emergency physicians. The relevance of diagnostic problems in the prehospital period of an AMI is unknown. We prospectively studied 421 patients seen by a primary care physician in the prehospital period of an AMI. Using a standardized interview, data were obtained to identify factors determining nonadmission. Of 421 AMI patients, 327 (77.7%) were directly admitted to hospital after examination by the physician, whereas 94 (22.3%) were not admitted. The median prehospital delay was 240 min in admitted and 2,200 min in nonadmitted patients. Using a stepwise logistic regression model, the following factors were identified as independent contributors to nonadmission: the patient not being much affected by the symptoms (2.48; 1.40–4.39), improvement of symptoms (2.59; 1.46–4.59), the patient not thinking to suffer an AMI (2.33; 1.28–4.17) and the patient being unable to imagine having a heart disease (1.93; 1.07–3.46). Conclusion: Nonadmission of AMI patients by health care professionals is a common problem. Several aspects of AMI presentation including the often limited intensity of symptoms and the variability of the clinical course may have to be re-emphasized by cardiologists. Taking a very careful history and being circumspect about the patient’s interpretation of symptoms still are the keys to a correct diagnosis of AMI.