Intraaortic Balloon Pump Counterpulsation, Part I: History, Technical Aspects, Physiologic Effects, Contraindications, Medical Applications/Outcomes.

Intraaortic balloon pump counterpulsation is the most common form of mechanical circulatory support used in patients with myocardial ischemia and cardiogenic shock. The physiologic principles of counterpulsation include diastolic augmentation of aortic pressure and systolic reduction of left ventricular afterload, resulting in hemodynamic benefits through increased coronary perfusion pressure and improved myocardial oxygen balance in patients with myocardial ischemia. Major trials have failed to conclusively demonstrate improvements in morbidity and mortality with counterpulsation therapy for patients with acute myocardial infarction (MI), cardiogenic shock, and/or severe coronary artery disease undergoing revascularization therapy, and the debate over its applications continues. Part I of this review focuses on the history of the development of counterpulsation, technical considerations, and complications associated with its use, its physiologic effects, and evidence for its use in myocardial ischemia and cardiogenic shock.

The History of Primary Angioplasty and Stenting for Acute Myocardial Infarction.

The evolution of the management of acute myocardial infarction (MI) has been one of the crowning achievements of modern medicine. At the turn of the twentieth century, MI was an often-fatal condition. Prolonged bed rest served as the principal treatment modality. Over the past century, insights into the pathophysiology of MI revolutionized approaches to management, with the sequential use of surgical coronary artery revascularization, thrombolytic therapy, and percutaneous coronary intervention (PCI) with primary coronary angioplasty, and placement of intracoronary stents. The benefits of prompt revascularization inspired systems of care to provide rapid access to PCI. This review provides a historical context for our current approach to primary PCI for acute MI.

Of MIs and men--a historical perspective on the diagnostics of acute myocardial infarction.

The history of myocardial infarction (MI) diagnostics has gone through a continuous evolution over the past century, when several new discoveries have contributed to remarkably increase the number of patients appropriately diagnosed with this condition. The tale "of MIs and Men" displays rather a long history, since atherosclerosis was found to be present in humans several centuries before modern civilization and the identification of the most prevalent risk factors. It was only at the end of the 19th century and at the beginning of the 20th century that the physicians acknowledged that MI is principally sustained by coronary thrombosis, and that the clinical picture of MI could be subsequently confirmed at autopsy. With the first description of the electrocardiogram (ECG) in the 1910s and 1920s, the history of modern MI diagnostics really began. Additional important discoveries followed, which are mainly represented by radiography, echocardiography, computed tomography, and magnetic resonance imaging of the heart. Another major breakthrough occurred at the down of the third millennium, with the development of commercial immunoassays for the measurement of cardiac troponin I and T, which represent now the cornerstones for identifying any kind of myocardial injury, thus including MI. The major advancements in the understanding of MI pathophysiology and the progressive introduction of efficient diagnostic tools will be described and discussed in this narrative historical review.

[To the centennial of the myocardial infarction. Priorities of domestic researchers in the study of the problem of modern cardiology].

There are domestic priorities in the 100-year history of myocardial infarction research a description of the disease clinical picture by V.P.Obrazcov and N.D.Strazhesko, development of mammary-coronary bypass by V.I.Kolesov, intracoronary thrombolysis by E.I.Chazov et al.

Concept of vulnerable/unstable plaque.

Today's concept of vulnerable plaque has evolved primarily from the early pioneering work uncovering the pivotal role of plaque rupture and coronary thrombosis as the major cause of acute myocardial infarction and sudden cardiac death. Since the first historical description of plaque rupture in 1844, several key studies by leading researchers and clinicians have lead to the current accepted views on lesion instability. Important to the complex paradigm of plaque destabilization and thrombosis are many discoveries beginning with the earliest descriptions of advanced plaques, reminiscent of abscesses encapsulated by fibrous tissue capable of rupture. It was not until the late 1980s that studies of remodeling provided keen insight into the growth of advanced plaques, beyond the simple accumulation of lipid. The emphasis in the next decade, however, was on a focused shift toward the mechanisms of lesion vulnerability based on the contribution of tissue proteolysis by matrix metalloproteinases as an essential factor responsible for thinning and rupture of the fibrous cap. In an attempt to unify the understanding of what constitutes a vulnerable plaque, morphological studies, mostly from autopsy, suggest the importance of necrotic core size, inflammation, and fibrous cap thickness. Definitive proof of the vulnerable plaque, however, remains elusive because animal or human data supporting a cause-and-effect relationship are lacking. Although emerging imagining technologies involving optical coherence tomography, high-resolution MRI, molecular biomarkers, and other techniques have far surpassed the limits of the early days of angiography, advancing the field will require establishing relevant translational animal models that produce vulnerable plaques at risk for rupture and further testing of these modalities in large prospective clinical trials.

After the triumph of cardiovascular medicine over acute myocardial infarction at the end of the 20th Century. -Can we predict the onset of acute coronary syndrome? (Con)-.

Predicting acute cardiovascular ischemic events is a crucial and urgent issue in the current cardiovascular field. An enormous effort to develop methodologies to achieve this purpose is being undertaken in cardiovascular institutes worldwide. However, currently, there is no established method of determining acute cardiovascular ischemic events in advance. This article reviews the latest progress on understanding how these events occur and how they can be detected. This goal represents a great dream that has realistic expectations.

The LDL receptor.

In this article, the history of the LDL receptor is recounted by its codiscoverers. Their early work on the LDL receptor explained a genetic cause of heart attacks and led to new ways of thinking about cholesterol metabolism. The LDL receptor discovery also introduced three general concepts to cell biology: receptor-mediated endocytosis, receptor recycling, and feedback regulation of receptors. The latter concept provides the mechanism by which statins selectively lower plasma LDL, reducing heart attacks and prolonging life.