Exercise produces profound alterations in symptoms and hemodynamics in patients with valvular aortic stenosis (AS). Prior studies have demonstrated marked increases in late left ventricular (LV) diastolic filling pressure with exercise. Little information is available on the exercise response of indexes of early LV diastolic performance. Catheter-tip manometer recordings in 11 patients with AS and 5 age-matched controls were obtained at rest and with supine bicycle exercise at the time of cardiac catheterization. Pressure-derived indexes of LV diastolic performance, isovolumic relaxation rate, and diastolic interval data were examined. At rest, early (patients 22 +/- 6 mm Hg, controls 12 +/- 3 mm Hg; p <0.01), minimal (patients 9 +/- 4 mm Hg, controls 4 +/- 1 mm Hg; p <0.01), and late (patients 28 +/- 10 mm Hg, controls 13 +/- 3 mm Hg; p <0.002) LV diastolic pressures were elevated in patients with AS. The time to onset of isovolumic relaxation (patients 422 +/- 31 ms, controls 363 +/- 40 ms; p <0.01) and minimal LV diastolic pressure (patients 608 +/- 57 ms, controls 448 +/- 52 ms; p <0.002) at rest were prolonged in patients with AS. With exercise, early (patients 45 +/- 14 mm Hg, controls 15 +/- 3 mm Hg; p <0.002), minimal (patients 15 +/- 6 mm Hg, controls 2 +/- 1 mm Hg; p <0.01), and late (patients 38 +/- 10 mm Hg, controls 18 +/- 5 mm Hg; p <0.002) LV diastolic pressures were elevated, and the time to minimal LV diastolic pressure (patients 528 +/- 26 ms; controls 393 +/- 56 ms) and peak first derivative of LV pressure decline (-LV dP/dt) (patients 395 +/- 41 ms, controls 326 +/- 59 ms) were prolonged in AS. furthermore, patients with AS failed to comparably increase the rate of LV pressure decay and isovolumic relaxation with exercise. The LV diastolic response to exercise in patients with AS is distinguished from the control response by suboptimal and prolonged relaxation and a diminished rate of LV pressure decay. These abnormal responses in early diastolic function coupled with the known abnormal chamber distensibility in AS contribute to significant elevations in early, mid-, and late diastolic pressures with exercise.

Transesophageal echocardiography (TEE) is a useful technique in the diagnosis and intraoperative assessment of discrete subaortic stenosis (DSS). It allows clear visualization of the subaortic membrane, which may be missed by transthoracic echocardiography, differentiates DSS from other causes of left ventricular outflow tract obstruction, and accurately detects the presence of associated aortic regurgitation and bacterial endocarditis. Limitations in its use include inadequate visualization of the left ventricular outflow tract by TEE in the presence of a prosthetic mitral valve or mitral annular calcification, and improper alignment of the Doppler cursor across the outflow tract.

Heparin-induced thrombocytopenia and thrombosis syndrome (type II) is associated with thromboembolic complications and a mortality rate up to 30%. We describe a patient who developed intracardiac and aortic Dacron prosthesis heparin-induced thrombosis after aortic root conservative surgery. Successive transoesophageal echocardiographies demonstrated a progressive regression of intracardiac thrombosis with oral anticoagulation by warfarin and antiplatelet therapy combining aspirin and clopidogrel.

L'ulcère pénétrant de l'aorte (UPA) est une ulcération siégeant au niveau de l'aorte qui peut entraîner une douleur brutale thoracique ou thoraco-abdominale. Le risque évolutif essentiel est la rupture aortique. Décrite pour la première fois en 1934, l'UPA n'a été pendant longtemps qu'une découverte nécropsique. A ce jour, l'angio scanner avec coupes fines représente l'examen de choix pour son diagnostic. Nous présentons, quinze cas d'UPA principalement symptomatiques ; sept cas présentaient une douleur brutale thoracique ou thoraco-abdominale, trois cas une douleur moins intense. Chez les cinq cas restant le diagnostic a été fortuit. L'intervention a consisté dans treize cas en la mis en place d'une ou plusieurs endoprothèses. Dans six cas un geste chirurgical complémentaire a été nécessaire, avec une technique hybride (pontage ilio-hépatique (un cas), pontages viscérales multiples (trois cas), pontage carotido-carotidien (un cas), pontage carotido-sous-clavière gauche (un cas) ou avec une technique combinée (anevrysmectomie de l'aorte sous rénale avec pontage aorto-aortique un cas). Dans deux cas, le traitement a été uniquement chirurgical classique : anastomose proximale dans la région thoraco-abdominale et distale sur le carrefour aortique. Les résultats immédiats ont été satisfaisants malgré un décès au quatorzième jour post-opératoire, dans un tableau de déchéance multi viscérale. Le suivi moyen est de 16,2 mois (maximum 44 mois) : un patient a développé au deuxième mois postopératoire une fistule aorto-aesophagienne entraînant son décès ; trois patients sont décédés : des suites d'un ictus dans un cas et pour raisons inconnues chez les deux autres. Les dix patients restants sont en bonne santé.Penetrating aortic ulcer (PAU) consists of an ulcer located in the aortic wall that can cause sudden-onset thoracic or thoraco-abdominal pain. Symptomatic PAU is a life-threatening emergency because of the high risk of aortic rupture. First described in 1934, PAU was for many years seen only at autopsy. Now, multislice CT is the diagnostic method of choice. We report the cases of 15 such patients. Ten patients were symptomatic, with severe suddenonset thoracic or thoraco-abdominal pain (7 cases) or less acute pain (3 cases). Surgical treatment consisted of aortic stent-grafting in 13 cases, with one or more endoprostheses. Bypass surgery was also necessary in 6 cases, using a hybrid technique (ilio-hepatic bypass graft in 1 case, multiple visceral bypass grafts in 3 cases, carotid-carotid bypass graft in 1 case, and carotid left subclavian bypass graft in 1 case), or a combined technique (aneurysmectomy and infrarenal Dacron tube repair in 1 case). Open thoraco-abdominal aortic repair was performed in two cases, with proximal anastomosis at the thoracoabdominal level and distal anastomosis at the level of the aortic carrefour (with the Crawford inclusion technique in one case). Perioperative results were satisfactory, but one patient died of multiple organ failure on postoperative day 14. Four patients died during follow-up (mean 16.2 months ; range 1-44 months), 1 of stroke, 1 of a complicated esophageal-aortic fistula, and 2 of unknown causes. Follow-up has been uneventful in the other 10 patients.

While Doppler echocardiography has become the gold standard for the diagnosis of hypertrophic cardiomyopathy, there are many pitfalls in its use. Some of these pitfalls are technical in nature resulting from inadequate image quality, incorrect transducer angulation, and improper equipment settings. Other pitfalls relate to the diversity and heterogeneity in defining hypertrophic cardiomyopathy and to the host of disorders that may mimic it by echocardiography. The pattern and extent of ventricular hypertrophy, systolic anterior motion of the mitral valve, andDoppler determination of left ventricular outflow tract obstruction, diastolic dysfunction, and mitral regurgitation are discussed, as are wall‐motion abnormalities and myocardial echo reflectivity. While these echocardiographic features of hypertrophic cardiomyopathy are nonspecific when seen in isolation, their combined presence in the appropriate clinical setting makes the diagnosis likely.

Diaphragmatic hernia may mimic a left atrial mass when imaged by transthoracic echocardiography. In this case study we emphasize the value of transesophageal echocardiography in clarifying the cause of this apparent atrial mass.

This retrospective study examines whether a relationship exists between the severity of mitral regurgitation (MR) and the presence of left atrial spontaneous echo contrast and/or thrombus (SEC/THR) as assessed by transesophageal echocardiography in 427 consecutive patients. Clinical data were evaluated in 316 of these patients. Nine percent of patients with MR < or = 2+ versus < 1% of those with MR > or = 3+ had SEC/THR (p < 0.03). Atrial fibrillation, left ventricular dysfunction, mitral stenosis, and mitral valve prosthesis were demonstrated to be independent positive predictors of left atrial SEC/THR, whereas MR > or = 3+ was an independent negative predictor of SEC/THR. SEC/THR was less common in patients with MR > or = 3+ than in patients with MR < or = 2+ for any given number of independent positive predictors of SEC/THR. This relationship did not hold true in patients with a mechanical mitral prosthetic valve. Clinical data revealed a trend towards a lower prevalence of stroke or transient ischemic attacks in patients with MR > or = 3+. Stroke and transient ischemic attacks were significantly more common in patients with SEC/THR (p < 0.001). We suggest that significant MR may be protective against the formation of left atrial SEC/THR.

We have previously shown that CsA administration to rats causes a high turnover bone loss with bone resorption exceeding bone formation. Similar findings have been reported in renal and cardiac transplantation patients administered CsA. Cyclosporine-G (CsG), a natural equipotent immunosuppressive analogue of CsA, has been shown to be less nephrotoxic than CsA. We therefore compared the effects of CsG and CsA on bone mineral metabolism. Sixty male Sprague-Dawley rats were divided into 3 equal groups as follows: group A (n = 20) was the control; group B (n = 20) received CsA 15 mg/kg by daily gavage; and group C received CsG 15 mg/kg by daily gavage for 28 days. Rats were bled weekly for measurement of circulating biochemical parameters of bone mineral metabolism and after sacrifice on day 28, the tibiae were removed for histomorphometric analysis. The tibial bone histomorphometry revealed that the percentage of bone volume was significantly reduced, and the osteoclast count increased in both the CsA and CsG group, but significantly less so in the CsG than the CsA group. Parameters reflecting bone formation in the CsG group were similar to controls but significantly different from the CsA group. Bone Gla protein levels in the CsA group were significantly increased compared with the control and CsG groups from day 14. Serum 1,25 dihydroxyvitamin D was increased significantly in the CsA group on days 14 and 28 compared with both control and CsG groups, and was significantly elevated in the CsG group compared with controls on the same days. We conclude that CsG is significantly less deleterious to bone mineral metabolism than CsA in the rat in vivo.

A patent foramen ovale (PFO) is an embryological remnant found in 27% of adults. It is a potential right-to-left intracardiac shunt. Shunting may be the result of reversal in the interatrial pressure gradient or abnormal streaming of blood in the right atrium. The pathologic consequences of right-to-left shunting include hypoxemia and paradoxical embolism. PFO may exacerbate preexisting hypoxemia or be its primary cause. Paradoxical embolism through a PFO is well documented. Its role in cryptogenic stroke remains controversial. A PFO may be detected by both invasive and noninvasive techniques. Contrast transesophageal echocardiography with provocative maneuvers is the diagnostic method of choice allowing visualization of the shunt. Patients with cryptogenic stroke should be screened for a PFO. If detected, noninvasive studies for deep vein thrombosis are recommended. Treatment must be tailored to the presentation. Surgical or transcatheter closure is recommended for hypoxemia. Prevention of venous embolism (air or thrombus) with or without closure of the PFO is recommended for paradoxical embolism.

We have previously shown that cyclosporin A (CsA) produces high bone remodeling with resorption exceeding formation and loss of bone volume in the rat. This may have important clinical implications where CsA is widely used in organ transplantation. 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) is a bone mineralizing hormone which also has immune modifying properties. Consequently, we studied the effect of combined CsA and 1,25(OH)2D3 administration over 28 days in four groups of rats. Group A received vehicle (n = 10), group B CsA (15 mg/kg) (n = 10) alone, group C 1,25(OH)2D3 plus CsA (n = 15), and group D 1,25(OH)2D3 alone (20 ng/100 g) (n = 15). Rats were bled periodically at day 0, 7, 14, and 28 and Ca, parathyroid hormone (PTH), 1,25(OH)2D, osteocalcin (bone Gla-protein, BGP), BUN, and creatinine were measured. Rats were sacrificed on day 28 and bones were examined histomorphometrically. Compared to controls, CsA resulted in significant elevation of BGP and a transient increase in 1,25(OH)2D with excess bone remodeling and loss of bone volume. 1,25(OH)2D3 administration produced hypercalcemia, a significant rise in BGP, with suppression of PTH and increased osteoid volume. Combined therapy prevented the loss of bone volume probably due to increased osteoid tissue and enhanced osteoblast activity. Renal dysfunction, a side-affect of CsA, was not a factor. In conclusion, 1,25(OH)2D3 combined with CsA restores bone volume which is accompanied by increases in serum calcium and BGP.

The mechanism of the acute hypocalcemia that follows acute ethanol administration has not been established. Measurements of parathyroid hormone (PTH) performed during this hypocalcemia reveal conflicting results. We compared the response of ionized calcium (Ca2+), immunoreactive PTH and bone Gla protein (BGP) after ethanol- and EDTA-induced hypocalcemia. 103 male Sprague Dawley rats each weighing approximately 300 g received ethanol and 100 rats of similar weight received EDTA. In each of these studies the animals were divided into experimental and control groups. The ethanol-treated rats received ethanol, 2 g/kg body weight, by ip injection and the EDTA-treated rats received 100 mg EDTA/kg body weight by im injection. Controls received normal saline by the corresponding route of administration. Rats were sacrificed at 0, 30, 60, 90, 180 and 360 min for the measurement of the above parameters. In both experimental groups Ca2+ levels were significantly reduced to the same degree by 30 min with return to control values by 360 min. There was no significant difference in immunoreactive PTH, and BGP between control and ethanol-treated groups. In the EDTA-treated rats, however, PTH values were significantly increased at 30 (P less than 0.005) and BGP at 60 and 90 minutes (P less than 0.005) vs. control. Therefore acute ethanol administration appears to blunt the PTH response to hypocalcemia. A direct inhibitory effect of ethanol on osteoblast function ie BGP production cannot be excluded. In addition, PTH may stimulate BGP.

Although cyclosporin A (CsA) and cortisone acetate (CRT) adversely affect bone, their combined effect on bone is unknown. Sprague Dawley rats were therefore administered either vehicle or CsA (7.5 mg/kg/day) by gavage and saline or CRT (2 mg/100 mg/day) by s.c. injection for 28 days. Group A received vehicle plus saline, group B CsA plus saline, group C vehicle plus CRT, and group D CsA/CRT. Serial bloods were sampled over a 28-day period for ionized calcium (Ca), PTH, 1,25 dihydroxyvitamin D (1,25(OH)2D), and bone gla protein (BGP osteocalcin) and tibia were examined on day 28 for histomorphometry. Results were compared with group A. Ca and PTH levels in groups B, C, and D were similar to those in group A during the study period. Group B had lower body weights, elevated levels of BGP, and an increase in 1,25(OH)2D. Group C developed weight loss and a decrease in BGP and 1,25(OH)2D. Group D had weight loss, BGP levels between those of group A and group C, and 1,25(OH)2D values similar to group A. Bone histomorphometry revealed high turnover osteopenia in group B and hyperostosis in group C with a decrease in bone formation and osteoclastlike cells. Combination therapy returned these to control values. In conclusion, the adverse effects of either CsA or CRT on bone in rats are minimized by combined therapy.

To prevent the high turnover bone remodeling associated with acute estrogen deficiency, the bisphosphonate [2-(2-pyridinyl) ethylidene-BP] (2-PEBP) was administered to oophorectomized (OX) rats. Three groups of 15 rats each (250 g) were studied. Group (Gp) A was sham operated, Gp B was OX, and Gp C received 2-PEBP (1.72 mg/kg/day) intraperitoneally for 3 days commencing 4 days postoophorectomy. Oophorectomy was confirmed with serum estradiol measurements. Blood samples were collected on days -7, 0, 7, 14, 21, and 28 for ionized calcium (Ca2+), PTH, and serum bone gla protein (BGP). Rats received tetracycline for bone histomorphometric labeling. All results were compared to Gp A. Body weight increased significantly in Gps B and C (P less than 0.005 by day 28). There was no significant difference in Ca2+, and PTH levels in Gps B and C were similar to Gp A. BGP levels were significantly higher on day 28 in Gp B (P less than 0.05). In Gp C, BGP levels were significantly decreased on days 7, 21, and 28 (P less than 0.03). Gp B revealed increased bone turnover without loss of bone volume (BV/TV). BV/TV was significantly increased in Gp C despite a decrease in parameters of bone formation and normal osteoclast number. In conclusion, 2-PEBP in the OX rat inhibited bone resorption more than formation with resultant hyperostosis. Serum BGP appeared to be a good marker of the changes observed on bone histomorphometry.