RESUMO
Coronary artery aneurysm (CAA) is an uncommon disease observed in only 0.15-4.9% of patients undergoing coronary angiography. CAA are defined as dilated coronary artery sections exceeding by 1.5 times the diameter of normal adjacent segments or of the patient's largest coronary vessel. Occasionally, CAA enlarge enough to be called giant CAA. We report the case of a 78-year-old man, with known chronic ischemic cardiomyopathy and a history of prior coronary artery bypass surgery (with a left internal mammary artery graft to the left anterior descending coronary artery and saphenous venous graft to the obtuse marginal branch), who was referred to our cardiology department for progressive dyspnea. Echocardiography showed severe mitral regurgitation suggesting replacement; coronary angiography revealed three-vessel coronary artery disease, left internal mammary artery patency, saphenous vein graft occlusion and an aneurysm of the mid right coronary artery. Cardiac magnetic resonance confirmed this finding, showing a giant CAA (65 x 75 mm) with a large endoluminal thrombus. Treatment is not standardized and may include medical therapy, percutaneous treatment and surgical intervention; our patient underwent percutaneous coil embolization. One-month angiographic follow-up showed successful obliteration. The patient underwent surgical mitral valve replacement without any complications. At 9-month clinical follow-up, he was asymptomatic; transthoracic echocardiography showed an ejection fraction of 44% without prosthetic mitral regurgitation.
Assuntos
Aneurisma Coronário/terapia , Embolização Terapêutica/métodos , Insuficiência da Valva Mitral/cirurgia , Idoso , Aneurisma Coronário/diagnóstico , Aneurisma Coronário/patologia , Angiografia Coronária , Ecocardiografia , Seguimentos , Implante de Prótese de Valva Cardíaca/métodos , Humanos , Imageamento por Ressonância Magnética , MasculinoRESUMO
Chronic angina represents a condition that impairs quality of life and is associated with decreased life expectancy in the industrialized countries. Current therapies that reduce angina frequency include old drugs such as nitrates, ß -blockers and calcium antagonists. Several new investigational drugs are being tested for the treatment of chronic angina. This review will focus on ranolazine, a drug approved by the US Food and Drug Administration (FDA) in 2006 for patients with chronic angina who continue to be symptomatic despite optimized therapies. The main molecular mechanism underlying ranolazine-mediated beneficial effects has been identified as inhibition of the late Na+ current during the action potential, which potentially improves oxygen consumption, diastolic dysfunction and coronary blood flow. The aim of this review is to update the evidence for ranolazine treatment in chronic angina and discuss its therapeutic perspectives based on the most recent clinical and experimental studies.
Assuntos
Angina Pectoris/tratamento farmacológico , Fármacos Cardiovasculares/uso terapêutico , Ranolazina/uso terapêutico , Bloqueadores dos Canais de Sódio/uso terapêutico , Angina Pectoris/metabolismo , Angina Pectoris/fisiopatologia , Animais , Fármacos Cardiovasculares/metabolismo , Fármacos Cardiovasculares/farmacocinética , Fármacos Cardiovasculares/farmacologia , Ensaios Clínicos Controlados como Assunto , Diástole/efeitos dos fármacos , Humanos , Ranolazina/metabolismo , Ranolazina/farmacocinética , Ranolazina/farmacologia , Bloqueadores dos Canais de Sódio/metabolismo , Bloqueadores dos Canais de Sódio/farmacocinética , Bloqueadores dos Canais de Sódio/farmacologiaRESUMO
Cardiovascular diseases and in particular coronary atherosclerotic disease are the leading cause of mortality and morbidity in the industrialized countries. Coronary atherosclerosis has been recognized for over a century and it was the subject of various studies. Pathophysiological studies have unravelled the interactions of molecular and cellular elements involved in atherogenesis; during the last decades the basic research has focused on the study of the instability of atherosclerotic plaque. Plaque rupture and resulting intracoronary thrombosis are thought to account for most acute coronary syndromes including ST - segment elevation myocardial infarction and non ST - segment elevation myocardial infarction. This is a brief review of the pathophysiology of atherosclerotic plaque development.
Assuntos
Artérias/fisiopatologia , Doença da Artéria Coronariana/complicações , Doença da Artéria Coronariana/fisiopatologia , Placa Aterosclerótica/complicações , Placa Aterosclerótica/fisiopatologia , Síndrome Coronariana Aguda/etiologia , Animais , Artérias/patologia , Doença da Artéria Coronariana/patologia , Vasos Coronários/patologia , Vasos Coronários/fisiopatologia , Humanos , Placa Aterosclerótica/patologia , Fatores de Risco , Trombose/etiologiaRESUMO
Cardiovascular disease and in particular, acute coronary syndromes are one of the principle causes of death in the industrialized countries. In the setting of acute coronary syndromes (both ST - segment or non ST - segment elevation myocardial infarction), platelets aggregation plays a key and central role in their development. Platelets are the mediators of hemostasis at sites of vascular injury, but they also mediate pathologic thrombosis; activated platelets stimulate thrombus formation in response to rupture of an atherosclerotic plaque or endothelial cell erosion promoting atherothrombotic disease. Recent patent relates to the methods and devices for treating atherosclerosis and to prevent in-stent restenosis or thrombosis. Because of the importance of platelets involvement in the initiation and propagation of thrombosis, antiplatelet drugs have a source of research; in the recent past, new antiplatelet drugs (such as ticagrelor) have been studied and placed in the routine therapy. The aim of this paper is to summarize the pharmacological properties and the clinical characteristics of ticagrelor.
Assuntos
Síndrome Coronariana Aguda/tratamento farmacológico , Adenosina/análogos & derivados , Antagonistas do Receptor Purinérgico P2Y/uso terapêutico , Síndrome Coronariana Aguda/fisiopatologia , Adenosina/farmacologia , Adenosina/uso terapêutico , Animais , Plaquetas/efeitos dos fármacos , Plaquetas/metabolismo , Doenças Cardiovasculares/tratamento farmacológico , Doenças Cardiovasculares/fisiopatologia , Humanos , Patentes como Assunto , Agregação Plaquetária/efeitos dos fármacos , Inibidores da Agregação Plaquetária/farmacologia , Inibidores da Agregação Plaquetária/uso terapêutico , Antagonistas do Receptor Purinérgico P2Y/farmacologia , Trombose/tratamento farmacológico , Trombose/patologia , TicagrelorRESUMO
Cardiovascular disease, in particular acute coronary syndromes (ACS), is still one of the leading causes of death in industrialized countries. ACS including ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI) and unstable angina pectoris (UA) are associated with lower mortality if diagnosed early. The diagnosis is based on clinical symptoms, ECG and circulating biomarker-level changes. Recent studies have shown that there are alternatives to the known biomarkers such as ultrasensitive troponin I or T and creatine kinase Mb; there are, in fact, novel biomarkers such as miRNAs. These are 22-nucleotide-long non-coding RNAs that regulate gene expression at post-transcriptional level. Several recent studies have shown that miRNAs play a physiological role in cardiovascular homeostasis and in the pathogenesis of cardiovascular disease. Expression-pattern studies of myocardial tissue reveal that several miRNAs are up- or down-regulated during myocardial infarction. The purpose of the present review is to highlight the state of the art and future views on this topic.
Assuntos
Síndrome Coronariana Aguda/diagnóstico , MicroRNAs/metabolismo , Infarto do Miocárdio/diagnóstico , Síndrome Coronariana Aguda/genética , Síndrome Coronariana Aguda/mortalidade , Angina Instável/diagnóstico , Angina Instável/genética , Angina Instável/mortalidade , Animais , Biomarcadores/metabolismo , Humanos , Peptídeos e Proteínas de Sinalização Intracelular , Infarto do Miocárdio/genética , Infarto do Miocárdio/mortalidade , Regulação para CimaRESUMO
Intra-aortic balloon counterpulsation is the most widely used form of mechanical hemodynamic support in the setting of cardiogenic shock due to ST-segment elevation myocardial infarction (STEMI). Intra-aortic balloon pump (IABP) is also strongly recommended (class 1b) in the current European guidelines for treatment of STEMI. The evidence of a possible benefit of IABP in this setting is based mainly on registry data and a few randomized trials. Cardiogenic shock and subsequent death due to STEMI result from three factors: hemodynamic deterioration, occurrence of multiorgan dysfunction and systemic inflammatory response. IABP does not cause an immediate improvement in blood pressure, but the recent SHOCK II trial shows positive effects on multiorgan dysfunction. Some experimental and clinical studies have indicated that IABP results in hemodynamic benefits as a result of afterload reduction and diastolic augmentation with improvement of coronary perfusion. However, the effect on cardiac output is modest and may not be sufficient to reduce mortality. Furthermore we can say that the use of IABP before coronary revascularization in the setting of STEMI complicated with cardiogenic shock may make the interventional procedure safer by improving left ventricular unloading. The purpose of the present review is to clarify the state of the art on this topic.
Assuntos
Balão Intra-Aórtico , Infarto do Miocárdio/terapia , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto , Sistema de Registros , Choque Cardiogênico/terapia , Resultado do TratamentoRESUMO
Coronary artery disease is the major cause of mortality and morbidity in the industrialized countries; in the United States of America and in Europe, it is responsible for one of every six deaths per year. In the setting of ischemic heart disease, angina pectoris and chest pain, in particular, are the major causes of emergency department accesses. Angina pectoris is a clinical syndrome characterized by discomfort typically in the chest, neck, chin and left arm induced by physical exertion, emotional stress and cold and is relieved by rest or by taking of nitrates. The main targets of treatment of angina pectoris are to improve quality of life by reducing the frequency and the severity of symptoms, to increase functional capacity and to improve prognosis. Ranolazine is a recent antianginal drug with unique methods of action. It was approved by the US Food and Drug Administration in 2006 as add-on therapy in patients symptomatic for stable angina. With the inhibition of the late sodium current, Ranolazine protects against ion deregulation, prevents cellular calcium overload and the subsequent increase in diastolic tension without impacting heart rate and blood pressure. Short term clinical trials and patent research show that add on therapy with Ranolazine in patients with chronic stable angina significantly improves exercise duration, exercise time to angina and reduces the use of nitro glycerine. Long term clinical trials showed no significant differences in the rate of cardiovascular death and myocardial infarction in patients with non-ST segment elevation acute coronary syndromes but a reduction in terms of recurrent ischemia. Ranolazine is generally well tolerated and even if it increases the duration of QTc interval it is not associated with atrial and ventricular arrhythmias. Therefore Ranolazine represents a good therapeutic approach in patients with chronic stable angina still symptomatic, while on optimal anti-ischemic therapy, or intolerant to traditional anti-ischemic drugs.
Assuntos
Acetanilidas/uso terapêutico , Isquemia Miocárdica/tratamento farmacológico , Piperazinas/uso terapêutico , Bloqueadores dos Canais de Sódio/uso terapêutico , Acetanilidas/efeitos adversos , Acetanilidas/farmacocinética , Acetanilidas/farmacologia , Angina Estável/tratamento farmacológico , Animais , Arritmias Cardíacas/tratamento farmacológico , Ensaios Clínicos como Assunto , Diabetes Mellitus/tratamento farmacológico , Interações Medicamentosas , Insuficiência Cardíaca/tratamento farmacológico , Humanos , Piperazinas/efeitos adversos , Piperazinas/farmacocinética , Piperazinas/farmacologia , RanolazinaRESUMO
Acute coronary syndromes and, in paticular, ST - segment elevation myocardial infarction are the principle causes or mortality and morbidity in the industrialized countries. The manadgement of acute myocadial infarction is much debated in the literature; primary percutaneous coronary intervention is the treatment of choice. In the recent years there has been an increasing interest in the concept of adjunctive pharmacological therapy to improve outcomes in primary percutaneous coronary intervention. In the literature randomized trials of intravenous or more recently intracoronary injection of glycoprotein IIb/IIIa inhibitors have provided conflicting results with no definitive evidence for efficacy. The aim of the report is to review the evidence to our date on the role of intracoronary injection of abciximab during primary percutaneous intervention in the setting of acute myocardial infarction.
Assuntos
Anticorpos Monoclonais/administração & dosagem , Fragmentos Fab das Imunoglobulinas/administração & dosagem , Infarto do Miocárdio/tratamento farmacológico , Intervenção Coronária Percutânea , Inibidores da Agregação Plaquetária/administração & dosagem , Complexo Glicoproteico GPIIb-IIIa de Plaquetas , Abciximab , Anticorpos Monoclonais/efeitos adversos , Quimioterapia Adjuvante , Humanos , Fragmentos Fab das Imunoglobulinas/efeitos adversos , Complexo Glicoproteico GPIIb-IIIa de Plaquetas/antagonistas & inibidoresRESUMO
During the last years an increasing number of patients with high perioperative risk and decreased left ventricular function are referred to cardiac and non-cardiac surgery. In this subgroup of patients, heart failure is the major cause of perioperative morbidity and mortality. In order to prevent and treat this type of complications several therapeutic attempts have been tried involving intra aortic balloon pump and inotropic agents infusion (such as beta-adrenergic agonists and phosphodiesterase inhibitors) Levosimendan is new inotropic agent; it is a calcium-sensitising inotropic agent and a vasodilator used in the treatment of heart failure. In the last ten years several reports have been published on levosimendan. The inotropic efficacy of levosimendan is dose-dependent and equal or even superior to any of the other commercially available inotropic agents. The aim of the present review is to describe experimental and clinical effects of perioperative treatment with levosimendan.
Assuntos
Procedimentos Cirúrgicos Cardíacos , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/cirurgia , Hidrazonas/uso terapêutico , Piridazinas/uso terapêutico , Vasodilatadores/uso terapêutico , Terapia Combinada , Humanos , Cuidados Pré-Operatórios , SimendanaRESUMO
CONTEXT: Data on the efficacy of beta-blockers in the 3 most common genetic long QT syndrome (LQTS) loci are limited. OBJECTIVE: To describe and assess outcome in a large systematically genotyped population of beta-blocker-treated LQTS patients. DESIGN, SETTING, AND PATIENTS: Consecutive LQTS-genotyped patients (n = 335) in Italy treated with beta-blockers for an average of 5 years. MAIN OUTCOME MEASURES: Cardiac events (syncope, ventricular tachycardia/torsades de pointes, cardiac arrest, and sudden cardiac death) while patients received beta-blocker therapy according to genotype. RESULTS: Cardiac events among patients receiving beta-blocker therapy occurred in 19 of 187 (10%) LQT1 patients, 27 of 120 (23%) LQT2 patients, and 9 of 28 (32%) LQT3 patients (P<.001). The risk of cardiac events was higher among LQT2 (adjusted relative risk, 2.81; 95% confidence interval [CI], 1.50-5.27; P =.001) and LQT3 (adjusted relative risk, 4.00; 95% CI, 2.45-8.03; P<.001) patients than among LQT1 patients, suggesting inadequate protection from beta-blocker therapy. Other important predictors of risk were a QT interval corrected for heart rate that was more than 500 ms in patients receiving therapy (adjusted relative risk, 2.01; 95% CI, 1.16-3.51; P =.01) and occurrence of a first cardiac event before the age of 7 years (adjusted RR, 4.34; 95% CI, 2.35-8.03; P<.001). CONCLUSION: Among patients with genetic LQTS treated with beta-blockers, there is a high rate of cardiac events, particularly among patients with LQT2 and LQT3 genotypes.