Dissociations between changes in myocardial cyclic adenosine monophosphate and contractility.

The relationship between changes in the myocardial concentration of adenosine 3':5'-cyclic monophosphate (cyclic AMP) and cardiac contractility was studied in guinea pig and rat myocardium. When isolated perfused guinea pig heart were perfused with 10-5-M papaverine, a potent inhibitor of cyclic AMP phosphodiesterase activity, myocardial cyclic AMP concentration increased significantly from 1.7 plus and minus 0.2 (SE) pmoles/mg protein (N equal 12) to 3.3 plus and minus 0.2 pmoles/mg protein (N equal 12), and the percent of phosphorylase aual 6) (P less than 0.01). However, perfusion with papaverine had no effect on contractility in the absence or the presence of exogenous epinephrine. In perfused rat hearts, 10-5 M glucagon increased myocardial cyclic AMP concentration from 1.5 plus and minus 0.1 pmoles/mg protein (N equal 12) to 2.6 plus and minus 0.1 pmoles/mg protein (N equal 12) (P less than 0.001). In contrast, cyclic AMP levels did not increase detectably in guinea pig heart perfused with glucagon. Glucagon increased adenylate cyclase activity more than twofold in rat myocardial broken cell preparations but failed to stimulate the enzyme in preparations from guinea pigs. Despite these differences, the positive inotropic effects of glucagon on rat and guinea pig hearts were very similar over a wide dose range. Thus, with both papaverine and glucagon, changes in cardiac contractility were dissociated from stimulation of adenylate cyclase activity, increases in myocardial cyclic AMP levels, and conversion of phosphorylase b to phosphorylase a in perfused hearts.     

Interaction between cyclic adenosine monophosphate and cyclic gunaosine monophosphate in guinea pig ventricular myocardium.

The purpose of this study was to examine the mechanisms underlying adrenergic-cholinergic antagonism in ventricular myocardium. Myocardial contractility, cyclic adenosine monophosphate (AMP) levels, and cyclic guanosine monophosphate (GMP) levels were measure in isolated guinea pig ventricles after treatment with various inotropic agents given alone and simultaneously with acetylcholine. Acetylcholine alone markedly elevated cyclic GMP levels but did not substantially change myocardial contractility. However, the same concentration of acetylcholine significantly attenuated the inotropic effect of isoproterenol and histamine, two drugs that may act by increasing myocardial levels of cyclic AMP. The decrease in the inotropic response to isoproterenol did not appear to be due to a decrease in the generation of cyclic AMP, because cyclic AMP levels were similar in hearts receiving isoproterenol alone and those receiving isoproterenol with acetylcholine. Dibutyryl cyclic GMP also antagonized the intropic action of isoproterenol. Acetylcholine did not alter the inotropic effects of ouabain, an agent that increases myocardial contractility without changing cyclic AMP levels. These results suggest that cyclic GMP mediates the antiadrenergic effects of acetylcholine by specifically antagonizing the inotropic actions of cyclic AMP.     

Effect of angiotensin II on cyclic guanosine monophosphate and cyclic adenosine monophosphate in human plasma.

Infusion of alpha-adrenergic catecholamines increases plasma cyclic guanosine monophosphate (pcGMP), raising the possibility that the pressor effect of these agents may be mediated by cyclic GMP. We infused pressor doses of angiotensin II in 10 studies in 8 normal subject and measured pcGMP and plasma cyclic adenosine monophosphate (pcAMP) by radioimmunoassay. After 120 minutes of infusion, mean pcGMP was 128 +/- 31% (SE) higher than baseline values (P less than 0.01) while pcAMP was increased 30 +/- 10% (P less than 0.05).     

Expression of cyclic adenosine monophosphate response-element binding protein in acute leukemia

Cyclic adenosine monophosphate response-element binding protein (CREB) is a nuclear protein that regulates expression of genes that control cell proliferation, differentiation, and survival. To analyze CREB expression in leukemia cells, we conducted Western blot analysis of bone marrow cells obtained from patients with acute lymphoblastic leukemia, patients with acute myeloid leukemia, and patients without active leukemia. CREB was expressed at a higher frequency in bone marrow cells from patients with acute lymphoid or myeloid leukemia than in patients with leukemia remission or without leukemia. Our results indicate that CREB expression could be a useful marker for leukemia in patients with acute disease and suggest a role for CREB in leukemogenesis.     

Catecholamine-dependent cyclic adenosine monophosphate and renin in the dog kidney.

Lithium inhibits the catecholamine-dependent cyclic adenosine monophosphate (AMP) generation in the kidney but not the hemodynamic effects of beta-adrenergic stimulation. Therefore, the possible role of catecholamine-dependent cyclic AMP in the release of renin was investigated in lithium-treated dogs both in vivo and vitro. Lithium therapy had no measurable effect on the increase in plasma renin activity induced by an injection of isoproterenol (2.6 plus and minus 1.2 (SE) ng/hour in control dogs vs. 3.0 plus and minus 1.2 ng/hour in lithium-treated dogs, P greater than 0.05). However, lithium inhibited the isoproterenol-induced increase in urinary excretion of cyclic AMP in vivo (791 plus and minus 199 pmoles/min in control dogs vs. 123 plus and minus 129 pmoles/min in lithium-treated dogs, P less than 0.05) and the increase in cyclic AMP concentration in renal tissue in vitro (4.50 plus and minus 0.15 pmoles/ng wet tissue in control dogs vs. 0.34 plus and minus 0.26 pmoles/mg in lithium-treated dogs, P less than 0.01). The finding that, in the lithium-treated dogs, isoproternol increased plasma renin activity but not cyclic AMP generation in the kidney suggests that the increase in plasma renin activity observed after an injection of isoproterenol is probably not mediated through the beta-adrenergic stimulus-dependent cyclic AMP system in the kidney.     

Mucinous digestive tumors. Case reports and review of the literature

We present three rare entities of mucinous tumors: appendiceal mucinous adenomas, enteroid mucinous cyst and pseudomyxoma peritonei, the latter as a developmental course or separate idiopathic etiology of mucinous tumors. We attempted to clarify the term of pseudomyxoma peritonei, a poorly understood condition, characterized by a diffuse intraperitoneal collection of gelatinous fluid with mucinous tumoral implants on the peritoneal surfaces. With this rare condition it is often difficult to establish the histological and developmental malignant or benign characteristics. We analyzed 4 patients admitted during the period of February 2000 - February 2002 in the First Surgical Clinic of St. Spiridon Hospital and in addition we referred to the current approach in the recent literature. In three of the four patients the diagnosis was possible preoperatively by imaging techniques and consequently they were operated by laparoscopic procedure for the complete removal of tumor cells at macroscopic level. We preferred to administrate chemotherapy accordingly to the malignant/ benign aspect, choosing the long term follow up of the patients to ward off the eventual relapse. We considered the future state of these cases to be uneventful, with a real chance of long term survival. In conclusion, the symptoms are not always specific, allowing errors in diagnosis. Imaging techniques offer real elements of diagnosis. Laparoscopic techniques could offer an oncologic approach with no less benefit compared to open surgery. This methodology also allows different surgery for a different pathology at the same time. The origin of these tumors is more frequently digestive and less ovarian.     

Atrial myxoma related myocardial infarction: Case report and review of the literature

Atrial myxomas are the commonest primary cardiac tumors and usually affect the left atrium. Patients with atrial myxomas present with intracardiac obstruction, embolization to the pulmonary and systemic circulation, or constitutional symptoms.The coronary arteries’ involvement in myxomatous embolization, although rare, has been described to cause acute myocardial infarction (AMI). We report a case of atrial myxoma associated MI and present the clinical and echocardiographic features of this presentation followed by review of the English literature for the association of atrial myxomas and acute myocardial infarctions (AMI).     

Non-coronary myocardial infarction in myasthenia gravis: Case report and review of the literature

Cardiovascular adverse events in patients with myasthenia gravis (MG) are rare, but the early recognition of such events is crucial. We describe a case of a noncoronary myocardial infarction (MI) during the initial treatment period with pyridostigmine bromide in a female patient with MG. Clinicians should be cautious about the appearance of potential MI in patients with MG. A baseline electrocardiogram is advocated, when the early recognition of the MI clinical signs and the laboratory findings (myocardial markers) are vital to the immediate and appropriate management of this medical emergency, as well as to prevent future cardio-vascular events. In this case report possible causes of myocardial adverse events in the context of MG, which may occur during the ongoing treatment and the clinical course of the disease, are discussed.     

Terlipressin-related acute myocardial infarction: a case report and literature review

Acute ST-segment elevation myocardial infarction after the administration of terlipressin in patients with hemorrhagic esophageal varices is a rare but life-threatening complication. We report the case of a 73-year-old female patient with esophageal variceal bleeding complicated with acute ST-segment elevation myocardial infarction after intravenous injection of terlipressin. We discuss the underlying mechanisms of terlipressin-related acute myocardial infarction and review the literature.     

Myocardial rupture in acute myocardial infarction: case report and review of the literature

Our patient demonstrates why the diagnosis of myocardial rupture is often mistaken for an extension of a myocardial infarction. Our case further suggests, as supported in the literature, that myocardial rupture is not an abrupt event. With close monitoring in patients with high risks, it is possible, especially with use of echocardiograms, to make an early diagnosis. Once the diagnosis is made, aggressive surgical therapy should be undertaken. With the advances in cardiovascular surgery, the prognosis of cardiac rupture is vastly improved. Long-term prognosis for patients surviving surgical repair after myocardial rupture is excellent. However, one should keep in mind the importance of preventive therapy such as treatment of systolic hypertension on admission to the coronary care unit.     

Essential thrombocythemia-related acute ST-segment elevation myocardial infarction. A case report and literature review

Essential thrombocythemia is a clonal disorder of the myeloid stem cell that causes pathologic expansion of the megakaryocytic elements in the bone marrow, with a persistent increase in the platelet count. The disease is associated with an elevated risk of thrombosis, hemorrhage, and vasomotor symptoms. The presenting features of essential thrombocythemia can range from being asymptomatic to thrombohemorrhagic complications including acute myocardial infarction. Acute ST-segment elevation myocardial infarction due to left main trunk and ostial left anterior descending coronary artery lesions was diagnosed in a young 31-year-old man. Platelet count was markedly increased and essential thrombocythemia was also diagnosed. Because of left main disease, primary coronary intervention was not feasible and an emergent coronary artery bypass grafting was performed along with pharmacologic management of essential thrombocythemia. The early postoperative period was complicated by acute pulmonary embolism. Hydroxyurea and anagrelide were administered postoperatively, resulting in the decrease of platelet count. A succinct review of myocardial infarction in patients with essential thrombocythemia is presented, and therapeutic strategies in such patients are discussed.     

Plasma cyclic adenosine 3'5'-monophosphate (AMP) levels in acute myocardial infarction

Plasma cyclic adenosine 3′5′-monophosphate (AMP) levels were measured in 44 patients with acute myocardial infarction, 33 patients with other cardiac and noncardiac diseases and 20 normal volunteers. The normal range of cyclic AMP was 4 to 16 picomoles/ml. The 35 surviving patients with acute myocardial infarction tended to have a slightly increased level of plasma cyclic AMP during the first 24 hours with a subsequent return to normal; the 9 nonsurvivors had abnormally high levels of cyclic AMP. An inverse correlation was found between cyclic AMP levels and stroke work index, and plasma cyclic AMP levels were of equal or better prognostic value than stroke work index. Plasma cyclic AMP levels were in the normal range in patients without acute myocardial infarction. Thus, very high levels of plasma cyclic AMP, found in patients with fatal myocardial infarction, appear to have clinical significance.     

Myocardial infarction associated with myocardial bridging: Case history and review of the literature

A 38-year-old male presented with an acute anterior myocardial infarction. Immediate cardiac catheterization revealed no evidence of angiographically significant atherosclerotic coronary artery disease, but there was a subtotal occlusion of the mid-left anterior descending coronary artery from myocardial muscle bridging. The patient did well with medical management. This review details myocardial bridging and its treatment. Cathet. Cardiovasc. Diagn. 40:364–367, 1997. © 1997 Wiley-Liss, Inc.