Performance of Coronary Artery Calcium Testing in Patients With Severe Psoriasis: Risk Assessment and Reclassification Potential in a Low Cardiovascular Risk Population / Realización del examen de calcio en los pacientes con psoriasis severa: evaluación del riesgo y potencial de reclasificación en una población de riesgo cardiovascular bajo

Background Patients with severe psoriasis have an increased cardiovascular (CV) risk and prevalence of subclinical coronary artery disease (CAD). Coronary artery calcium (CAC) testing can detect subclinical CAD and improve cardiovascular risk assessment beyond clinical scores. Objectives Evaluate the presence and magnitude of subclinical CAD determined by CAC score among the different ESC/EAS CV risk categories, as well as the potential for risk reclassification, in patients with severe psoriasis from a low CV risk population. Methods Unicentric cross-sectional study in 111 patients with severe chronic plaque psoriasis from a low CV risk population in the Mediterranean region. Patients were classified into four CV risk categories according to the ESC/EAS guideline recommendations and HeartScore/SCORE calibrated charts. Patients underwent coronary computed tomography to determine their CAC scores. Patients in the moderate-risk category with a CAC score of ≥100 were considered to be reclassified as recommended by the 2019 ESC/EAS guidelines. Reclassification was also considered for patients in the low-risk category with a CAC score>0. Results Presence of subclinical CAD was detected in 46 (41.4%) patients. These accounted for 86.2% of patients in high/very-high-risk categories and 25.6% of patients in non-high-risk categories. Fourteen (17.1%) of the patients in non-high-risk categories were reclassifiable due to their CAC score. This percentage was higher (25%) when considering the moderate-risk category alone and lower (13.8%) in the low-risk category. Age was the only variable associated with presence of subclinical CAD and reclassification. Conclusions Over 40% of patients with severe psoriasis from a low-risk region and up to 25% of those in non-high-risk categories have subclinical CAD (AU)

Antecedentes Los pacientes con psoriasis severa tienen riesgo cardiovascular (CV) incrementado, así como prevalencia de la enfermedad de las arterias coronarias (EAC) subclínica. El examen de calcio en las arterias coronarias (CAC) puede detectar la EAC subclínica y mejorar la evaluación del riesgo CV más allá de las puntuaciones clínicas. Objetivos Evaluar la presencia y magnitud de la EAC subclínica determinadas mediante la puntuación CAC entre las diferentes categorías de riesgo CV de ESC/EAS, así como el potencial de reclasificación del riesgo, en pacientes con psoriasis severa, procedentes de una población de riesgo CV bajo. Métodos Estudio transversal unicéntrico de 111 pacientes con psoriasis crónica en placa procedentes de una población de bajo riesgo CV de la región mediterránea. Los pacientes fueron clasificados en cuatro categorías de riesgo CV conforme a las recomendaciones de la guía ESC/EAS y la tabla de calibración HeartScore/SCORE. Se realizó a los pacientes una tomografía computarizada para determinar sus puntuaciones CAC. Se consideró que los pacientes de la categoría de riesgo moderado con una puntuación CAC≥100 debían ser reclasificados, conforme a las guías ESC/EAS de 2019. También se reconsideró la reclasificación para aquellos pacientes de la categoría de riesgo bajo con una puntuación CAC>0. Resultados La presencia de EAC subclínica fue detectada en 46 pacientes (41,4%), que representaron el 86,2% de los pacientes incluidos en las categorías de riesgo alto/muy alto, y el 25,6% de los pacientes de las categorías de riesgo no alto. Catorce pacientes (17,1%) de las categorías de riesgo no alto no fueron reclasificables debido a su puntuación CAC. Este porcentaje fue más alto (25%) al considerar la categoría de riesgo moderado en solitario, y más bajo (13,8%) en la categoría de riesgo bajo. La edad fue la única variable asociada a la presencia de EAC subclínica y reclasificación (AU)

[Artículo traducido] Realización del examen de calcio en los pacientes con psoriasis severa: evaluación del riesgo y potencial de reclasificación en una población de riesgo cardiovascular bajo / Performance of Coronary Artery Calcium Testing in Patients With Severe Psoriasis: Risk Assessment and Reclassification Potential in a Low Cardiovascular Risk Population

Antecedentes Los pacientes con psoriasis severa tienen riesgo cardiovascular (CV) incrementado, así como prevalencia de la enfermedad de las arterias coronarias (EAC) subclínica. El examen de calcio en las arterias coronarias (CAC) puede detectar la EAC subclínica y mejorar la evaluación del riesgo CV más allá de las puntuaciones clínicas. Objetivos Evaluar la presencia y magnitud de la EAC subclínica determinadas mediante la puntuación CAC entre las diferentes categorías de riesgo CV de ESC/EAS, así como el potencial de reclasificación del riesgo, en pacientes con psoriasis severa, procedentes de una población de riesgo CV bajo. Métodos Estudio transversal unicéntrico de 111 pacientes con psoriasis crónica en placa procedentes de una población de bajo riesgo CV de la región mediterránea. Los pacientes fueron clasificados en cuatro categorías de riesgo CV conforme a las recomendaciones de la guía ESC/EAS y la tabla de calibración HeartScore/SCORE. Se realizó a los pacientes una tomografía computarizada para determinar sus puntuaciones CAC. Se consideró que los pacientes de la categoría de riesgo moderado con una puntuación CAC≥100 debían ser reclasificados, conforme a las guías ESC/EAS de 2019. También se reconsideró la reclasificación para aquellos pacientes de la categoría de riesgo bajo con una puntuación CAC>0. Resultados La presencia de EAC subclínica fue detectada en 46 pacientes (41,4%), que representaron el 86,2% de los pacientes incluidos en las categorías de riesgo alto/muy alto, y el 25,6% de los pacientes de las categorías de riesgo no alto. Catorce pacientes (17,1%) de las categorías de riesgo no alto no fueron reclasificables debido a su puntuación CAC. Este porcentaje fue más alto (25%) al considerar la categoría de riesgo moderado en solitario, y más bajo (13,8%) en la categoría de riesgo bajo. La edad fue la única variable asociada a la presencia de EAC subclínica y reclasificación (AU)

Background Patients with severe psoriasis have an increased cardiovascular (CV) risk and prevalence of subclinical coronary artery disease (CAD). Coronary artery calcium (CAC) testing can detect subclinical CAD and improve cardiovascular risk assessment beyond clinical scores. Objectives Evaluate the presence and magnitude of subclinical CAD determined by CAC score among the different ESC/EAS CV risk categories, as well as the potential for risk reclassification, in patients with severe psoriasis from a low CV risk population. Methods Unicentric cross-sectional study in 111 patients with severe chronic plaque psoriasis from a low CV risk population in the Mediterranean region. Patients were classified into four CV risk categories according to the ESC/EAS guideline recommendations and HeartScore/SCORE calibrated charts. Patients underwent coronary computed tomography to determine their CAC scores. Patients in the moderate-risk category with a CAC score of ≥100 were considered to be reclassified as recommended by the 2019 ESC/EAS guidelines. Reclassification was also considered for patients in the low-risk category with a CAC score>0. Results Presence of subclinical CAD was detected in 46 (41.4%) patients. These accounted for 86.2% of patients in high/very-high-risk categories and 25.6% of patients in non-high-risk categories. Fourteen (17.1%) of the patients in non-high-risk categories were reclassifiable due to their CAC score. This percentage was higher (25%) when considering the moderate-risk category alone and lower (13.8%) in the low-risk category. Age was the only variable associated with presence of subclinical CAD and reclassification. Conclusions Over 40% of patients with severe psoriasis from a low-risk region and up to 25% of those in non-high-risk categories have subclinical CAD (AU)

Performance of Coronary Artery Calcium Testing in Patients With Severe Psoriasis: Risk Assessment and Reclassification Potential in a Low Cardiovascular Risk Population.

BACKGROUND: Patients with severe psoriasis have an increased cardiovascular (CV) risk and prevalence of subclinical coronary artery disease (CAD). Coronary artery calcium (CAC) testing can detect subclinical CAD and improve cardiovascular risk assessment beyond clinical scores. OBJECTIVES: Evaluate the presence and magnitude of subclinical CAD determined by CAC score among the different ESC/EAS CV risk categories, as well as the potential for risk reclassification, in patients with severe psoriasis from a low CV risk population. METHODS: Unicentric cross-sectional study in 111 patients with severe chronic plaque psoriasis from a low CV risk population in the Mediterranean region. Patients were classified into four CV risk categories according to the ESC/EAS guideline recommendations and HeartScore/SCORE calibrated charts. Patients underwent coronary computed tomography to determine their CAC scores. Patients in the moderate-risk category with a CAC score of ≥100 were considered to be reclassified as recommended by the 2019 ESC/EAS guidelines. Reclassification was also considered for patients in the low-risk category with a CAC score>0. RESULTS: Presence of subclinical CAD was detected in 46 (41.4%) patients. These accounted for 86.2% of patients in high/very-high-risk categories and 25.6% of patients in non-high-risk categories. Fourteen (17.1%) of the patients in non-high-risk categories were reclassifiable due to their CAC score. This percentage was higher (25%) when considering the moderate-risk category alone and lower (13.8%) in the low-risk category. Age was the only variable associated with presence of subclinical CAD and reclassification. CONCLUSIONS: Over 40% of patients with severe psoriasis from a low-risk region and up to 25% of those in non-high-risk categories have subclinical CAD. CAC appears to be useful for reclassification purposes in CV risk assessment of patients with severe psoriasis. Further research is required to elucidate how CAC could be implemented in everyday practice at outpatient dermatology clinics dedicated to severe psoriasis.

Neoangiogenesis with endothelial precursors for the treatment of ischemia.

In the embryo, blood vessels and hematopoietic cells arise from the hemangioblast, a common precursor cell. Compelling evidence suggests that bone marrow from adult individuals contains endothelial cell precursors (EPCs), similar to embryonic hemangioblast. They are able to increase neovascularization of tissue after ischemia. Herein we have discussed the ontogeny of these cells, their phenotypes, and their isolation from various sources. We also have presented experimental studies indicating that EPCs are able to induce neovascularization and angiogenesis when transplanted into ischemic tissues. Furthermore, endogenous EPCs can be mobilized using factors that promote their homing to sites of tissue injury. We also have discussed the ongoing clinical trials using these cells to treat ischemic diseases.

U-46619-induced potentiation of noradrenergic constriction in the human saphenous vein: antagonism by thromboxane receptor blockade.

OBJECTIVE: We investigated the potentiating effect of U-46619, a synthetic analogue of thromboxane A(2) (TXA(2)), on the adrenergic responses in human saphenous vein. METHODS: Saphenous vein rings were obtained from 35 patients undergoing coronary artery bypass surgery. The rings were suspended in organ bath chambers for isometric recording of tension. RESULTS: U-46619 (10(-10)-3 x 10(-7) mol/l) produced concentration-dependent and endothelium-independent contractile responses. U-46619 (10(-10) mol/l) potentiated the contractions elicited by electrical stimulation and potassium chloride, and produced leftward shifts of the concentration-response curve for noradrenaline. The TXA(2) receptor antagonist SQ-30741 (10(-8) mol/l) prevented the potentiation evoked by U-46619. The dihydropyridine calcium antagonist nifedipine (10(-6) mol/l) did not affect the potentiation of electrical stimulation and noradrenaline induced by U-46619, but abolished the potentiation of U-46619 on KCl-induced contractions. CONCLUSIONS: U-46619 facilitates sympathetic neurotransmission and potentiates constrictor effects of noradrenaline in human saphenous veins through stimulation of TXA(2) receptors. These effects are independent of calcium entry through dihydropyridine calcium channels.

Hemoperitoneo por rotura de aneurisma de la arteria esplénica / Hemoperitoneum due to ruptured aneurysm of the splenic artery

Objetivo. Presentar 3 casos de hemoperitoneo secundario a rotura de aneurismas de la arteria esplénica (AAE) atendidos en el Servicio de Cirugía del Hospital Clínico Universitario de Valencia. Evaluar la rentabilidad de las exploraciones complementarias en relación a los hallazgos operatorios y el curso postoperatorio. Pacientes y métodos. Han sido intervenidos quirúrgicamente 3 pacientes (edad media de 48 años; r: 3161 años) por rotura de AAE. La manifestación clínica inicial fue dolor en hipocondrio izquierdo de aparición súbita, con signos de shock hipovolémico posteriormente (hipotensión, palidez y sudación).Resultados. Entre los estudios complementarios, tanto la hemoglobina como el hematócrito fueron normales en 2 de los 3 casos al ingreso. La ecografía abdominal, realizada en dos de los casos, evidenció un líquido libre intraabdominal determinando la etiología en uno de ellos. En 2 casos, el diagnóstico etiológico se confirmó mediante TC abdominal. La detección de hemorragia en la transcavidad de los epiplones es indicativo de rotura del aneurisma y signo de alarma previo al establecimiento del hemoperitoneo ("fenómeno de la doble rotura"). Sólo en uno de los casos se realizó una arteriografía que confirmó el diagnóstico pero que no logró ser terapéutica. En los tres pacientes se practicó aneurismectomía con esplenectomía, asociando pancreatectomía caudal en 2 de los casos, sin mortalidad postoperatoria. Conclusiones. El shock hipovolémico de etiología incierta es una forma frecuente de presentación de los AAE. En pacientes hemodinámicamente estables la TC es el método diagnóstico de elección e identifica precozmente las complicaciones hemorrágicas de los AAE y permite establecer una indicación de laparotomía urgente. El tratamiento de elección es la aneurismectomía, con esplenectomía y pancreatectomía, si técnicamente se precisa, según la localización del aneurisma (AU)

Relaxation induced by cGMP phosphodiesterase inhibitors sildenafil and zaprinast in human vessels.

BACKGROUND: Sildenafil is currently used in the treatment of erectile dysfunction. However, assessment of direct effects of sildenafil on coronary arteries and on arteries used as coronary grafts is unknown. This study was designed to investigate the effects of sildenafil on contracted human coronary, internal mammary, and radial arteries obtained from multiorgan donors. The observations were extended to forearm veins. Zaprinast was included in this study for comparison. METHODS: Segments of left coronary, internal mammary, and radial arteries, and forearm veins were obtained from 16 multiorgan donors. Vascular rings were suspended in organ bath chambers and isometric tension was recorded. Then the effects of sildenafil, zaprinast, and sodium nitroprusside on precontracted vessels were studied. RESULTS: Sildenafil (10(-8) - 3 x 10(-5) mol/L) caused concentration-dependent relaxation in the internal mammary arteries, radial arteries, and forearm veins. In the coronary arteries, sildenafil had a modest relaxant effect. In addition, sildenafil amplified the relaxation induced by sodium nitroprusside in all four vessels. Relaxation was unaffected by the inhibitor of nitric oxide synthase NG-monomethyl-L-arginine (10(-4) mol/L). Compared with zaprinast, sildenafil was eight to ten times more potent in terms of EC50 values. CONCLUSIONS: The direct relaxant effects of sildenafil together with its synergistic interaction with nitric oxide donors should be considered in patients undergoing coronary bypass surgery, patients with low blood pressure, and patients receiving antihypertensive regimes.

Contractile effects of arginine analogues on human internal thoracic and radial arteries.

OBJECTIVES: Plasma levels of endogenous guanidino-substituted analogues of L -arginine are increased in various pathologic conditions. In the present study we determined the effects of some of these compounds on basal and stimulated release of nitric oxide in human internal thoracic and radial arteries. METHODS: Rings of human internal thoracic and radial arteries were obtained from 16 multiorgan donors. The rings were suspended in organ baths for isometric recording of tension. RESULTS: N(G)-monomethyl L -arginine (10(-6) to 10(-3) mol/L) and N(G),N(G)-dimethyl L -arginine (10(-6) to 10(-3) mol/L) caused concentration- and endothelium-dependent contractions. Maximal force of contractions for N(G)-monomethyl L -arginine and N(G),N(G)-dimethyl L -arginine in the internal thoracic artery were 18.0% +/- 4.3% and 17.8% +/- 3.8%, respectively, of the contraction to 100 mmol/L KCl, and those found in the radial artery were 9.6% +/- 2.5% and 9.1% +/- 2.4%, respectively. Aminoguanidine (10(-5) to 3 x 10(-3) mol/L) and methylguanidine (10(-5) to 3 x 10(-3) mol/L) produced endothelium-independent contractions. L -Arginine (10(-3) mol/L) prevented the contractions by N(G)-monomethyl L -arginine and N(G),N(G)-dimethyl L -arginine but did not change contractions induced by aminoguanidine and methylguanidine. N(G)-monomethyl L -arginine and N(G),N(G)-dimethyl L -arginine inhibited, in a concentration-dependent manner, the endothelium-dependent relaxation to acetylcholine in the internal thoracic artery and had little attenuating effect in the radial artery; aminoguanidine and methylguanidine were without effect. CONCLUSIONS: The results suggest that the contractions induced by N(G)-monomethyl L -arginine and N(G),N(G)-dimethyl L -arginine are due to inhibition of both basal and stimulated nitric oxide production, whereas aminoguanidine and methylguanidine do not affect the synthesis of nitric oxide. An increase in the plasma concentration of N(G)-monomethyl L -arginine and N(G),N(G)-dimethyl L -arginine is likely to represent a risk factor for abnormal vasomotor tone in conduit arteries used as coronary grafts.

Effects of sildenafil on human penile blood vessels.

OBJECTIVES: To investigate the effects of sildenafil on human penile blood vessels and evaluate the interaction of sildenafil with neurogenic-mediated responses. Sildenafil is currently used in the treatment of erectile dysfunction. METHODS: Penile dorsal arteries and deep dorsal veins were obtained from 14 multiorgan donors. Vascular rings were suspended in organ bath chambers, and the isometric tension was recorded. We then studied the effects of sildenafil on precontracted vessels and the neurogenic (noradrenergic and nitrergic) responses. RESULTS: Sildenafil (10(-9) to 3 x 10(-6) M) caused concentration-dependent relaxation and amplified the relaxation induced by sodium nitroprusside. Relaxation was unaffected by the inhibitor of nitric oxide synthase N(G)-monomethyl-L-arginine (10(-4) M). Compared with zaprinast, sildenafil was 8 to 10 times more potent in terms of the median effective concentration (EC(50)) values. Electrical field stimulation of the vessels under resting tension caused frequency-dependent contractions that were attenuated in the presence of sildenafil. When penile vessels were contracted after blockade of norepinephrine release with guanethidine (10(-6) M), electrical stimulation induced frequency-dependent, nitric oxide-dependent relaxations that were enhanced by sildenafil. CONCLUSIONS: These results indicate that the relaxation of human penile arteries and veins induced by sildenafil involves inhibition of noradrenergic contraction, enhancement of neurogenic nitric oxide-mediated relaxation, and inhibition of smooth muscle contraction.

Comparative effects of dilator drugs on human penile dorsal artery and deep dorsal vein.

The present study was designed to characterize the response of human penile dorsal artery and deep dorsal vein to dilator drugs used in the diagnosis and treatment of erectile dysfunction with special emphasis on the effects on sympathetic neurotransmission. Ring segments of penile dorsal artery and deep dorsal vein were obtained from 20 multi-organ donors during procurement of organs for transplantation. The rings (3 mm long) were suspended in organ bath chambers for isometric recording of tension. We then studied the relaxant responses to prostaglandin E1 (PGE1), vasoactive intestinal peptide (VIP), papaverine (PV), sodium nitroprusside (SNP) and linsidomine chlorhydrate (SIN-1), and analysed the effects of these drugs on contractions induced by stimulation of perivascular sympathetic nerves. In artery and vein rings contracted by noradrenaline, all the drugs tested caused concentration-dependent relaxation. The order of potencies in terms of IC50 values (concentration of agonist causing 50% of the maximal relaxation) was PGE1=VIP>SNP>SIN-1=PV. Both arteries and veins contracted to electrical field stimulation (15 V, 0.5-2 Hz, 0.2 ms duration for 15 s) in a frequency-dependent manner. All relaxant drugs caused concentration-dependent inhibition of neurogenic contractions; the relative order of potencies was PGE1>VIP>SNP>SIN-1=PV. It is concluded that inhibition of sympathetic activity constitutes an effective relaxing mechanism in penile dorsal artery and vein. Modulation of sympathetic activity together with the direct effects on smooth muscle should be considered to evaluate adequately the efficacy of relaxant drugs to increase human penile blood supply.

Role of vasopressin on adrenergic neurotransmission in human penile blood vessels.

We have used in vitro preparations of human penile dorsal artery and deep dorsal vein from 20 multiorgan donors to investigate whether subpressor concentrations of vasopressin facilitate noradrenergic transmission in penile blood vessels. Vasopressin constricted penile dorsal arteries (pD2, 9.38 +/- 0.18) and deep dorsal veins (pD2, 9. 40 +/- 0.14) by activating V1 receptors. Vasopressin (10(-11) and 3 x 10(-11) M) caused concentration-dependent potentiation of the contractions elicited by electrical stimulation (15 V, 0.5-2 Hz, 0.2 msec duration for 15 sec) and produced leftward shifts of the concentration-response curve for norepinephrine. The V1 receptor antagonist d(CH2)5Tyr(Me)AVP (3 x 10(-9)-10(-7) M) induced concentration-dependent inhibitions of potentiation caused by vasopressin. In contrast, the V2 receptor antagonist [d(CH2)5,D-Ile2, Ile4,Arg8]-vasopressin (10(-8)-10(-7) M) did not prevent the potentiation induced by vasopressin. The results demonstrate that vasopressin exerts powerful constrictor action in human penile arteries and veins by direct stimulation of V1 receptors. In addition, vasopressin strongly potentiates the contractions to norepinephrine and stimulation of perivascular adrenergic nerves. Consequently, the direct contractile effects of vasopressin together with its amplifying effects on adrenergic-mediated constriction should be taken into consideration in the overall regulation of penile erection and in those states characterized by increased plasma vasopressin levels.

Neurogenic contraction and relaxation of human penile deep dorsal vein.

1. The aim of the present study was to characterize neurogenic and pharmacological responses of human penile deep dorsal vein and to determine whether the responses are mediated by nitric oxide from neural or endothelial origin. 2. Ring segments of human penile deep dorsal vein were obtained from 22 multiorgan donors during procurement of organs for transplantation. The rings were suspended in organ bath chambers for isometric recording of tension. We then studied the contractile and relaxant responses to electrical field stimulation and to vasoactive agents. 3. Electrical field stimulation (0.5-2 Hz) and noradrenaline (3 x 10(-10)-3 x 10(-5) M) caused frequency- and concentration-dependent contractions that were of greater magnitude in veins denuded of endothelium. The inhibitor of nitric oxide synthesis NG-nitro-L-arginine methyl ester hydrochloride (L-NAME, l0(-4) M) increased the adrenergic responses only in rings with endothelium. 4. In preparations contracted with noradrenaline in the presence of guanethidine (10(-6) M) and atropine (10(-6) M), electrical stimulation induced frequency-dependent relaxations. This neurogenic relaxation was prevented by L-NAME, methylene blue (3 x 10(-5) M) and tetrodotoxin (10(-6) M), but was unaffected by removal of endothelium. 5. Acetylcholine (10(-8)-3 x 10(-5) M) and substance P (3 x 10(-11) -3 x 10(-7) M) induced endothelium-dependent relaxations. In contrast, sodium nitroprusside (10(-9)-3 x 10(-5) M) and papaverine (10(-8) 3 x 10(-5) M) caused endothelium-independent relaxations. 6. The results provide functional evidence that the human penile deep dorsal vein is an active component of the penile vascular resistance through the release of nitric oxide from both neural and endothelial origin. Dysfunction in any of these sources of nitric oxide should be considered in some forms of impotence.

Arginine vasopressin enhances sympathetic constriction through the V1 vasopressin receptor in human saphenous vein.

BACKGROUND: Arginine vasopressin (AVP) not only acts directly on blood vessels through V1 receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments in vivo and in vitro. The aim of the present study was to investigate whether AVP can contribute to an abnormal adrenergic constrictor response of human saphenous veins. METHODS AND RESULTS: Saphenous vein rings were obtained from 32 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. AVP (3x10[-9] mol/L) enhanced the contractions elicited by electrical field stimulation at 1, 2, and 4 Hz (by 80%, 70%, and 60%, respectively) and produced a leftward shift of the concentration-response curve to norepinephrine (half-maximal effective concentration decreased from 6.87x10[-7] to 1.04x10[-7] mol/L; P<.05). The V1 vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP (10[-6] mol/L) prevented the potentiation evoked by AVP. The selective V1 receptor agonist [Phe,2 Orn8]-vasotocin (3x[-10]-9 mol/L) induced potentiation of electrical stimulation-evoked responses, which was also inhibited in the presence of the V1 receptor antagonist (10[-6] mol/L). In contrast, the V2 receptor agonist desmopressin (10[-9] to 10[-7] mol/L) did not modify neurogenic responses, and the V2 receptor antagonist [d(CH2)5, D-Ile,2 Ile,4 Arg8]-vasopressin (10[-8] to 10[-6] mol/L) did not prevent the potentiation induced by AVP. The dihydropyridine calcium antagonist nifedipine (10[-6] mol/L) did not affect the potentiating effect of AVP. CONCLUSIONS: The results suggest that low concentrations of AVP facilitate sympathetic neurotransmission and potentiate constrictor effects of norepinephrine in human saphenous veins. These effects appear to be mediated by V1 receptor stimulation and are independent of calcium entry through dihydropyridine calcium channels. Thus, AVP may contribute to vascular mechanisms involved in acute ischemic syndromes associated with venous grafts, particularly if the sympathetic nervous system is activated.

Subperiosteal new bone formation in association with vascular graft sepsis.

Hypertrophic osteoarthropathy (HOA) is a clinical and radiologic syndrome that consists of periosteal new bone formation, synovitis, and digital clubbing. Secondary HOA has been reported confined to one or two extremities that are perfused by Dacron grafts that have become infected. Herein we include a report of a vascular graft infection that shares some of the clinical features with HOA and a brief review of pathophysiologic theories. We conclude emphasizing that periostitis and other HOA signs and symptoms may play a role as a clue to support the suspicion of vascular graft infection when confusing and vague clinical features are present.

Endothelium-dependent relaxation of human saphenous veins in response to vasopressin and desmopressin.

PURPOSE: The goal of this study was to determine the effects of vasopressin and the selective V2-receptor agonist desmopressin on human saphenous veins, with special emphasis on endothelium-mediated responses. METHODS: Human saphenous vein segments were obtained from 35 patients undergoing coronary bypass surgery. Paired segments, one normal and the other deendothelized by gentle rubbing, were mounted for isometric recording of tension in organ baths. Concentration-response curves to vasopressin and desmopressin were determined in the presence and in the absence of either the V1-receptor antagonist d(CH2)5Tyr (Me)AVP (10(-6) mol/L), the V1-V2-receptor antagonist desGly-d(CH2)5D-Tyr(Et)ValAVP (10(-6) mol/L), indomethacin (10(-6) mol/L), or NG-nitro-L-arginine methyl ester hydrochloride (L-NAME, 10(-4) mol/L). RESULTS: In vein rings under resting tension, vasopressin produced concentration-dependent, endothelium-independent contractions with a concentration of vasopressin producing half-maximal contractions (EC50) of 3.44 x 10(-8) mol/L. The vasopressin V1-receptor antagonist (10(-6) mol/L) displaced the control curve to vasopressin 9.86-fold to the right in a parallel manner. In precontracted vein rings previously treated with the V1-antagonist (10(-6) mol/L) vasopressin caused endothelium-dependent relaxations. This relaxation was reduced significantly by indomethacin (10(-6) mol/L) and unaffected by the V1-V2-receptor antagonist (10(-6) mol/L) or by L-NAME (10(-4) mol/L). Desmopressin caused endothelium-dependent relaxations in precontracted vein rings that were inhibited by the mixed V1-V2-receptor antagonist and by indomethacin, but not by the V1-antagonist or by pretreatment with L-NAME. CONCLUSIONS: These observations indicate that vasopressin exerts contractile effects on human saphenous vein by V1-receptor stimulation. Vasopressin causes dilatation of human saphenous vein only if V1-receptor blockade is present. This relaxation appears to be mediated by the release of relaxant prostaglandins, probably derived from endothelial cells, and is independent of V2-receptor stimulation or release of nitric oxide. Desmopressin elicits relaxation that is largely dependent on V2-receptor stimulation, which may bring about the release of dilating prostaglandins from the endothelial cells.

[Cardiac angiosarcoma]. / Angiosarcoma cardíaco.

We report a case of a 29-year-old patient with recurrent hemorrhagic pericardial effusion secondary to a right atrial mass detected by transthoracic echocardiography. A more detailed anatomic study was provided by transesophageal echocardiogram and nuclear magnetic resonance imaging. During surgery, a biopsy confirmed the diagnosis of angiosarcoma. We discuss the contribution of echocardiography and other noninvasive methods to evaluate intracardiac tumors. A brief review of treatment and prognosis is made.

Kent bundle visualized in situ at operation after unsuccessful radiofrequency ablation.

Kent bundles are seldom visualized at operation, but, in the patient described, the pathway was subepicardial, running superficial to the right coronary artery. This was probably why radiofrequency ablation failed. When this unusual pathway course is encountered, the epicardial approach should be used at operation.

[Arterial embolisms in the upper and lower limbs: a clinical review]. / Embolias arteriales en miembros superiores e inferiores: revisión clínica.

A clinical review about the subjects is made. Percentages and comparisons between lower and upper limbs were established. Correlation with statistics from other authors are presented.

Myocardial protection by retrograde cardioplegic perfusion in the presence of acute coronary artery obstruction. An experimental study.

To investigate retrograde delivery of cardioplegic solutions as a means of enhancing myocardial protection in the presence of coronary artery occlusion, a two-part experimental model was devised. In part 1 (in vitro) the possibility of retroperfusing the entire myocardium during acute occlusion of the left anterior descending artery (LAD) was assessed. In part 2 (in vivo) acute LAD occlusion was performed in dogs, and during 2 hours of aortic cross-clamping crystalline cardioplegic solution was infused at 20-minute intervals. In group I the infusion was antegrade, via the aortic root, and in group II it was retrograde, via the coronary sinus. Thereafter the LAD snare was released and the dogs were weaned from bypass. Delivery of cardioplegia through the aortic root was associated with depression of ventricular function, poor myocardial cooling and severe cellular damage. With the retrograde procedure there was significantly improved recovery of left ventricular function, uniform myocardial cooling and better preservation of cellular morphology.