The association of dynamic left ventricular outflow tract obstruction and pheochromocytoma is rare with only about fifteen previously reported cases in the literature. The association may be the result of chronic increased catecholamine secretion which induces intra-ventricular obstruction in a hypertrophied ventricle due to hypertension. The authors report a new case in which the intraventricular gradient on Doppler echocardiography was particularly high at 120 mmHg. The gradient totally regressed after removal of the pheochromocytoma. The finding of a systolic murmur in a patient with pheochromocytoma should lead to the prescription of Doppler echocardiography and diagnosis of left ventricular tract obstruction must lead to the association of betablocker and alphablocker therapy before surgery. The removal of the pheochromocytoma is usually followed by the complete regression of left intraventricular obstruction, as in this case.

Serum myoglobin (Mb) was assayed by immuno-nephelemetry or immuno-turbidimetry together with creatinine kinase activity (CK) by spectrophotometry in 290 consecutive patients admitted to hospital between January 1st and September 30th 1992 in three cardiology departments for chest pain suggesting myocardial infarction (MI). The measurements were made at admission (T0) and 90 minutes later (T90). On admission, patients were classified as certain MI (N = 62), possible MI (N = 107) or definitely not MI (N = 121) and, on discharge, as certain MI (N = 144) or definitely not MI (N = 146). At T0, for a threshold value of 90 mcg/l, Mb assay had a sensitivity of 49.3% and a specificity of 95.2%, a positive predictive value of 91.8% and a negative predictive value of 65.6%. Increasing the threshold of positivity to 130 mcg/l was accompanied by a significant loss of sensitivity (38.2%) without any change in the other parameters. At T90, for a threshold value of 90 mcg/l, Mb assay had a sensitivity of 81.7%, a specificity of 92%, a positive predictive value of 89.5% and a negative predictive value of 85.8%. The increase in sensitivity between T0 and T90 made Mb assay very useful for correctly classifying the initial false negative results (20/28: 71.4%) and for diagnosing the possible MI (27/32: 84.4%). Decreasing the threshold of positivity to 80 or even to 70 mcg/l did not improve the diagnostic value of this test. The sensitivity of Mb assay was significantly higher than that of CK at T0 (49.3% vs 26.4%: p < 0.0001) and at T90 (81.7% vs 48.9%: p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Previous small clinical trials have suggested that treatment with nitric oxide donors in suspected myocardial infarction can reduce mortality by 30-35%. To confirm this finding in a large-scale trial, we compared molsidomine and its active metabolite linsidomine (a nitric oxide donor) with placebo in 4017 patients with acute myocardial infarction.In our trial, patients without signs of overt heart failure (Killip III/lV) were randomly assigned in a double-blind design within 24 h of symptom onset to receive linsidomine 1 mg/h intravenously for 48 h, followed by 16 mg molsidomine by mouth daily for 12 days (n = 2007), or an identical placebo (n = 2010). All other treatments could be used at the responsible physician's discretion with the exception of systematic vasodilator treatment. The molsidomine and placebo groups showed similar all-cause 35-day mortality (168 [8.4%] vs 176 [8.8%] deaths, p = 0.66), and adjustment for baseline variables in a Cox model had no effect. Similarly, we found no difference for long-term mortality(mean follow-up 13 months; 294 [14.7%] vs 285 [14.2%] deaths, p = 0.67). The two groups showed similar frequencies of major and minor adverse events; only headache was significantly more common in the molsidomine group.Changes in treatment practices and the lower risk profile of our study subjects than of participants in previous trials may explain the results. It is still not clear whether nitric oxide donors can improve survival in higher-risk myocardial infarction patients.

Serum myoglobin (Mb) was assayed by immuno-nephelemetry or immuno-turbidimetry together with creatinine kinase activity (CK) by spectrophotometry in 290 consecutive patients admitted to hospital between January 1st and September 30th 1992 in three cardiology departments for chest pain suggesting myocardial infarction (MI). The measurements were made at admission (TO) and 90 minutes later (T90). On admission, patients were classified as certain MI (N = 62), possible MI (N = 107) or definitely not MI (N = 121) and, on discharge, as certain MI (N = 144) or definitely not MI (N = 146).At TO, for a threshold value of 90 mcg/l, Mb assay had a sensitivity of 49.3 % and a specificity of 95.2 %, a positive predictive value of 91.8 % and a negative predictive value of 65.6 %. Increasing the threshold of positivity to 130 mcg/l was accompanied by a significant loss of sensitivity (38.2 %) without any change in the other parameters.At T90, for a threshold value of 90 mcg/l, Mb assay had a sensitivity of 81.7 %, a specificity of 92 %, a positive predictive value of 89.5 % and a negative predictive value of 85.8 %. The increase in sensitivity between T0 and T90 made Mb assay very useful for correctly classifying the initial false negative results (20/28 71.4 %) and for diagnosing the possible MI (27/32: 84.4 %). Decreasing the threshold of positivity to 80 or even to 70 mcg/l did not improve the diagnostic value of this test.The sensitivity of Mb assay was significantly higher than that of CK at TO (49.3 % vs 26.4 %: p < 0.0001) and at T90 (81.7 % vs 48.9 % : p < 0.0001). On the other hand, the specificity, the positive and negative predictive values of the two tests were similar.Mb assay by nephelemetry or turbidimetry is therefore a more sensitive parameter than that of CK for the early diagnosis of myocardial infarction ; it is accurate, rapid, and may easily be performed as an emergency. The result is usually available about 30 minutes after blood sampling. If the inital Mb value is normal, it would seem useful to repeat the test 90 minutes later to improve the diagnostic sensitivity of this marker.

The aim of this study was to determine whether the percentage of akinesia on echocardiography during the acute phase of transmural anterior myocardial infarction could predict secondary left ventricular dilatation. The study group comprised 24 patients (18 men and 6 women) with an average age of 59 years. The patients underwent two echocardiographic examinations, the first during the acute (< 72 hours) phase and the second, 6 months later. Ventricular volumes were calculated by the ellipse monoplane method in the apical 4 chamber view. The percentage of akinesia was defined as the ratio between the length of the akinetic segment and the left ventricular end diastolic perimeter in the apical 4 chamber view. An increase in end diastolic volume (83 +/- 25 vs 62 +/- 18 ml/m2; p < 0.01) and in end systolic volume (51 +/- 27 vs 34 +/- 11 ml/m2; p < 0.01) was observed 6 months after infarction without a significant change in ejection fractions (42 +/- 17% vs 44 +/- 10%). The percentage of akinesia in the acute phase was > 30% in 15 patients (Group I) and < 30% in 9 patients (Group II). The increase in ventricular volumes at 6 months after infarction was significant in Group I (p < 0.02) but not in Group II. At 6 months after infarction, the end systolic volumes were greater (60 +/- 27 vs 37 +/- 22 ml/m2, p < 0.5) and the ejection fractions were lower (35 +/- 13% vs 53 +/- 18%, p < 0.01) in Group I than in Group II.(ABSTRACT TRUNCATED AT 250 WORDS)

The association of a myocardial bridge of the left anterior descending (LAD) coronary artery and myocardial infarction is rare. The mechanisms by which the myocardial bridge could predispose to myocardial infarction are tachycardia (reducing the duration of diastolic coronary filling), thrombosis at the site of the myocardial bridge, and coronary spasm which, however, has never been demonstrated in the context of infarction. The aim of this study was to detect coronary spasm by provocative ergometrine testing in 4 patients, all male, aged 21 to 49 years, average 39 years old, who had anterior myocardial infarction associated with myocardial bridging of the LAD artery without atheromatous coronary stenosis. The ergometrine tests were performed during (2 cases) or after coronary angiography (2 cases). The systolic narrowing due to the myocardial bridge ranged from 25 to 95% (average 70%). The ergometrine test was strongly positive in 1 patient and negative in the other 3. Repermeabilisation of a thrombus was suggested in these 3 patients by the recording of an accelerated idioventricular rythm in the acute phase of infarction (2 cases) or by the demonstration of abnormal platelet aggregation (1 case). This is the first report of coronary spasm in a patient with myocardial bridging associated with infarction. However, it is not possible to determine the respective roles of spasm and myocardial bridging in the genesis of the infarct. We suggest systemic provocative ergometrine testing in this situation to orientate the most appropriate treatment.

A case of painless anteroseptal and high lateral wall infarction presenting as cardiogenic shock with pulmonary oedema 24 hours after childbirth complicated by severe post partum haemorrhage with a coagulation defect, is reported. Coronary angiography performed one month later was normal, with a negative ergometrine provocation test. The authors review five previous reports in the medical literature, and discuss the possible physiopathological mechanisms which, alone or in association could have operated in the reported case.

A case is reported in which, contrary to the unusual finding, conduction was slower in an accessory pathway than in the node-His pathway. Only when this latter became blocked (in the trunk of the bundle of His) following on the longest refractory period, was a pre-excitation syndrome unmasked related to the right nodo-ventricular fibres (the fibres of Mahaim).