Hemodynamic performance of cryopreserved aortic homograft valves during midterm follow-up.

OBJECTIVES: The aim of this prospective study of adult patients operated with a cryopreserved aortic homograft was to use serial echocardiographic data to evaluate the postoperative hemodynamic performance of these valves. BACKGROUND: Only limited data on hemodynamic performance of aortic homografts at rest and during exercise are available. Controversy also exists regarding incidence and progression of aortic regurgitation (AR). METHODS: Fifty-nine patients aged 39-86 years who received an aortic homograft (median size 21 mm) implanted with subcoronary technique were studied with serial Doppler-echocardiography (D-E). In 31 of these patients, D-E also was performed during supine exercise. RESULTS: Overall survival was 100% during a median follow-up of 28 months (range 4-54). During follow-up AR grade II or more was detected in 25% of the patients with an increasing time-related risk of developing AR. Maximum and mean pressure differences at 7 months follow-up calculated with the short form of the Bernoulli equation were 11.4 (4.6) and 5.5 (2.1) mm Hg, respectively. During supine exercise that increased cardiac output 72%, maximum pressure difference increased from 11.9 (5.2) to 18.5 (9.5) mm Hg. CONCLUSIONS: The aortic homograft valve shows low pressure differences at rest and during exercise, but AR grade I or II is often seen during follow-up. As AR progresses with time we stress the importance of echocardiographic follow-up of patients with aortic homografts.

Cyclo-oxygenase products released by low pH have capsaicin-like actions on sensory nerves in the isolated guinea pig heart.

OBJECTIVE: Previous work has shown that ischaemia releases calcitonin gene related peptide (CGRP) from capsaicin sensitive nerve terminals in the perfused heart. Prostacyclin (PGI2) is also released during ischaemia. The aim of this study was to investigate whether the release of CGRP by low pH and lactic acid was associated with PGI2 formation and if PGI2 mediated its effect through capsaicin receptors which could be inhibited by capsazepine. METHODS: The isolated Langendorff perfused guinea pig heart was used with a constant perfusion pressure of 70 cm H2O. Low pH was accomplished by changing the Tyrode solution to buffers with pH 7, 6, and 5, or lactic acid (5 mM with pH 6.9). The outflow of CGRP and the stable PGI2 metabolite 6-keto-PGF1 alpha was measured by radioimmunoassay. RESULTS: Low pH (pH 7, 6, 5) and lactic acid evoked release of CGRP. At moderate acidosis (pH 7 and 6) the CGRP release was dependent on extracellular Ca2+, while at pH 5 approximately half of the peptide release persisted in the absence of extracellular Ca2+. This release was attenuated by diclofenac or indomethacin, two inhibitors of prostaglandin formation, as well as by the capsaicin receptor antagonist capsazepine. Both arachidonic acid and PGI2, the predominant cyclo-oxygenase product formed during myocardial ischaemia, evoked a capsazepine sensitive release of CGRP, while capsazepine did not influence the formation of PGI2 evoked by low pH or arachidonic acid. CONCLUSIONS: In the isolated guinea pig heart, moderate acidosis is associated with CGRP release dependent on influx of extracellular Ca2+ and formation of PGI2, with subsequent stimulation of capsazepine sensitive receptors. With more severe acidosis there is an additional non-PGI2-linked CGRP release. Capsazepine represents a novel pharmacological principle for inhibiting the effects of prostanoids on sensory nerves without influencing their formation.

Calcitonin gene-related peptide in myocardial ischaemia and reperfusion in the pig.

OBJECTIVE: In myocardial ischaemia, slow conducting capsaicin-sensitive C-fibres are activated. Apart from the mediation of pain, activation of these fibres causes release of various peptides, such as calcitonin gene-related peptide (CGRP), which is a potent vasodilator. The aim of this study was to investigate the role of CGRP in the context of myocardial ischaemia in vivo. METHODS: The left anterior descending coronary artery (LAD) was occluded during 45 min in 27 anaesthetised open-chest pigs. LAD flow, mean arterial pressure (MAP), heart rate, peak dP/dt, arterial and coronary venous concentration of CGRP was measured prior to ischaemia, and during 4 h of reperfusion. The extent of myocardial infarction was measured using staining with triphenyl tetrazolium chloride. RESULTS: Retroinfusion of CGRP (100 micrograms) into the ischaemic myocardium was associated with a more pronounced hyperaemia, and systemic hypotension, during early reperfusion. The infarct size in relation to the area at risk was not affected by CGRP or the CGRP antagonist CGRP(8-37), and averaged 67 +/- 3%. There were no changes in plasma CGRP levels during ischaemia or reperfusion. CONCLUSION: Exogenously administered CGRP can cause systemic hypotension and augments postischaemic coronary flow. In this model, no cardioprotective effect of CGRP could be proven.

Recurrent factitious hypercalcemia.

Severe hypercalcemia recurred three times during an observation period of 15 years in a woman with anorexia nervosa. The patient displayed a factitious cheese-alkalosis syndrome similar to the iatrogenic milk-alkali syndrome.

Myocardial injury after electrical therapy for cardiac arrhythmias assessed by troponin-T release.

Episodes of ventricular fibrillation with subsequent intracardiac, and to a lesser extent, external defibrillation give rise to a statistically significant increase in S-troponin T, S-CK-MB(mass) and S-myoglobin indicative of a minor myocardial injury or dysfunction. In contrast, no such signs were observed after external direct-current conversion of atrial fibrillation using high energies, or after pace-terminated ventricular tachycardia.

Myocardial outflow of calcitonin gene-related peptide in relation to metabolic stress during coronary artery bypass grafting without cardiopulmonary bypass.

OBJECTIVE: Because of adverse effects of cardiopulmonary bypass and the prospect of shortening intensive care and hospital stay, coronary artery bypass grafting without cardiopulmonary bypass is gaining increased attention. The impact of the localized myocardial ischemia that is inherent in these procedures has not been thoroughly investigated in human beings. We have investigated metabolic changes, possible myocardial damage, and myocardial outflow of the vasodilator calcitonin gene-related peptide during coronary artery bypass grafting without cardiopulmonary bypass. METHODS: Coronary sinus and arterial blood was sampled before coronary arterial occlusion, after 10 minutes of ischemia, and after 1 and 10 minutes of reperfusion in 9 consecutive patients (mean age 70 +/- 5 years) who had an anastomosis performed to the left anterior descending artery without cardiopulmonary bypass. RESULTS: No perioperative myocardial infarctions occurred. The arteriovenous difference in lactate decreased during ischemia, to reach a minimum after 1 minute of reperfusion (-0.17 +/- 0.25 vs 0.15 +/- 0.25 mmol/L before ischemia; P =.008). Myocardial lactate extraction decreased (from 11.2 +/- 13.6 micromol/min before ischemia to -3.0 +/- 7.0 micromol/min after 1 minute of reperfusion; P =.012), that is, a net production of lactate. The arteriovenous difference in calcitonin gene-related peptide decreased from -0.1 +/- 2.6 pmol/L before ischemia to -30.5 +/- 26.5 pmol/L (P =.008) after 1 minute of reperfusion. CONCLUSIONS: The localized myocardial ischemia associated with these procedures causes metabolic changes in the myocardium, but no myocardial damage. The ischemia-related outflow of calcitonin gene-related peptide indicates that the vasodilating and cardioprotective properties of this peptide that are known from animal studies may be of importance in myocardial ischemia in human beings.

Transaortic approach for the Alfieri stitch.

The management of associated mitral regurgitation in patients undergoing cardiac surgery is controversial. A simple, reliable, and fast repair is advantageous, especially in critically ill patients. We describe a simple method of transaortic edge-to-edge repair in patients with associated mitral regurgitation undergoing aortic valve surgery.

Simple method for direct cannulation of ascending aortic aneurysms.

A simple method for direct cannulation of aneurysms of the ascending aorta is described. It avoids the need for femoral artery cannulation and offers an easy route for retrograde cerebral perfusion during deep hypothermic circulatory arrest.

Ion channels involved in the release of calcitonin gene-related peptide by low pH, prostacyclin and capsaicin in the isolated guinea-pig heart.

The aim of this study was to characterise the release of calcitonin gene-related peptide (CGRP) by capsaicin, low pH and prostacyclin in terms of Ca2+ channel dependence, interactions with K(ATP) channels and the role of action potential propagation, in the isolated, perfused guinea-pig heart. The Ca2+ channel blocker omega-conotoxin reduced CGRP release evoked by 10(-7) M capsaicin, as well as CGRP release evoked by pH 7. CGRP release caused by capsaicin at low (10(-7) M) but not high (10(-6) M) concentrations was also attenuated by tetrodotoxin, indicating partial dependence on action potential propagation. CGRP release caused by prostacyclin was not altered by any of the tested drugs. The K(ATP) channel activator cromakalim and the K(ATP) channel blocker glibenclamide had no effect on CGRP release. Previous findings that low pH and capsaicin stimulate capsaicin-sensitive afferents in the isolated heart at least partly through common mechanisms are thus supported. Attenuation of capsaicin-evoked release of CGRP by tetrodotoxin suggests recruitment of additional nerve terminals by a local axon reflex.

Capsazepine-sensitive release of calcitonin gene-related peptide from C-fibre afferents in the guinea-pig heart by low pH and lactic acid.

The present study aimed to evaluate the possible influence of the selective capsaicin antagonist, capsazepine, on the release of calcitonin gene-related peptide (CGRP)-like immunoreactivity from sensory nerves in the isolated perfused guinea-pig heart. Low-pH buffer (pH 7, 6, 5), capsaicin (10(-7) M), lactic acid (5, 20, 50 mM) and nicotine (10(-4) M) all evoked a clear-cut release of CGRP-like immunoreactivity. Incubation with capsazepine (10(-6) to 10(-5) M) significantly reduced the CGRP-like immunoreactivity release evoked by low pH, capsaicin and lactic acid (5 mM) but not that evoked by nicotine. Furthermore, the capsaicin-evoked stimulation of heart rate was inhibited by incubation with capsazepine. The inorganic dye, ruthenium red, which has previously been shown to attenuate capsaicin-, but not nicotine-induced CGRP release from the heart, also reduced the release of CGRP caused by low pH and lactic acid (5 mM). It is concluded that the CGRP-like immunoreactivity release evoked from the heart by low pH and lactic acid shares several characteristic features with the release evoked by capsaicin. Since tissue pH is low in myocardial ischaemia and this is well known to cause pain, the use of capsazepine to inhibit the function of C-fibre afferents may represent a novel principle to influence autonomic reflex reactions associated with cardiac pathological conditions.

Dual-energy X-ray absorptiometry registers bone mineral in the liver.

OBJECTIVE: To analyse the difference in bone mineral content (BMC) between the left and right trunk generally obtained by dual-energy X-ray absorptiometry (DXA) by creating identical images over the liver region and the contralateral side. PATIENTS AND DESIGN: Fifty-four patients were selected at random from 1,722 subjects examined by DXA because of osteoporosis. Another five patients were selected who had been followed for osteoporosis by repeated DXA two to five times at intervals from 2 to 36 months. One healthy volunteer was followed for one day by means of DXA total body measurements. All protocols were analysed with respect to BMC, fat mass (FM) and lean tissue mass (LTM) of the imaged trunk and liver. RESULTS: BMC of the right trunk exceeded that of the left trunk in 78% of the investigated subjects. The right (liver) image dominated in all 81 investigations calculated from 60 subjects. There were intraindividual short- and longterm variations between repeated DXA examinations. The amounts of FM and LTM were distributed symmetrically between the right and left trunk. CONCLUSIONS: DXA registers BMC in the liver, which explains the general dominance of the right trunk. The absorption over the liver region varies in the same individual in repeated measurements at intervals of hours to months.