For this Review, each contributing author selected references that he viewed as most relevant for his particular topic.
ReviewCardiovascular remodelling in coronary artery disease and heart failure
Introduction
“The heart is the beginning of life, for it is by the heart the blood is moved…the source of all action”, wrote William Harvey in 1673. The concept that such action could vary and the heart undergo remodelling in disease stretches back to the classic writings of Corvisart in 1806, when he described “two types of dilatation, active with thick walls and increased force of contraction, and passive with thinning of the walls and a decreased force of contraction”. These notions correspond to current concepts of left ventricular hypertrophy and dilatation as two contrasting types of cardiac remodelling. Yet we have to wait till 1984 before the then novel term remodelling more precisely described the early and later structural changes that occurred in infarcted and non-infarcted ventricular myocardium after coronary artery ligation.1 The next conceptual advance was that disproportionate thinning and dilatation occurred in the infarct region, accompanied by remote remodelling of non-infarcted myocardium, correlated with the extent of expansion. By 2000 the topic was sufficiently prominent to merit a consensus review document from the International Forum on Cardiac Remodelling. Patients with major remodelling underwent progressive worsening of cardiac function, and slowing or reversal of remodelling became a new goal of heart failure therapy.2
Originally, the term remodelling was proposed to characterise the response of remote myocardium to regional infarction and the progression from acute myocardial infarction to chronic heart failure.1, 3 Independently and at about the same time, the term remodelling was also used to characterise the progression of atherosclerotic vascular lesions.4, 5 In our Review, we advocate the concept of remodelling in a broader and more general sense to characterise the responses of myocardium and vasculature to potentially noxious haemodynamic, metabolic, and inflammatory stimuli, a process that is initially functional, compensatory, and adaptive in nature but, when sustained, progresses to structural changes that become self-perpetuating and pathogenic. Remodelling involves not only responses of the specific cardiovascular cells—cardiomyocytes, endothelium, smooth muscle cells—but also the interstitial cells and matrix.
Section snippets
Endothelial remodelling
The endothelial cell, positioned at the interface between the blood vessels and tissues, stands poised to sense the environment and signal modulations of vascular function to maintain homoeostasis and host defences against microbial invaders and injury.6 Inappropriate signalling from vascular endothelial cells can also contribute to common diseases characterised by arterial remodelling, notably atherosclerosis and hypertension. Endothelial cells sense the environment in two major ways: local
Coronary microvascular dysfunction and remodelling in ischaemic and reperfused myocardium
Remodelling of the epicardial coronary arteries has preoccupied clinical cardiologists because constrictive remodelling often yields stenotic plaques that cause chronic myocardial ischaemia, whereas expansive remodelling characterises plaques that rupture and provoke acute thromboses. The reperfusion era brought substantial changes in the management of acute myocardial infarction. The relief of symptoms in stable coronary artery disease and the prognosis of acute coronary syndromes have
Remodelling after myocardial reperfusion injury
Acute myocardial infarction is a major cause of death and disability worldwide. Much of this morbidity and mortality relates to the remodelling that occurs post infarction. Although cardiac remodelling is often associated with events that occur in the weeks and months after an acute myocardial infarction, its consequences invariably relate to the initial size of the associated infarction. Therefore optimum positive remodelling after a severe acute ischaemia–reperfusion event can improve patient
Myocardial remodelling in heart failure
Factors such as loading conditions, neurohormonal activation patterns, genetic background, and comorbid conditions affect the size, shape, and ultrastructure of the heart. In conditions such as pregnancy or endurance exercise terms such as physiological, adaptive, beneficial, or compensated remodelling are used, whereas during pathological stimulation by pressure or volume overload, the condition is described as maladaptive or decompensated remodelling.74 The phenotype, including ventricular
Impaired mitochondrial oxidative metabolism and adverse energetic remodelling of the failing heart
In addition to structural remodelling, remodelling of cardiac energy metabolism can contribute to the severity of heart failure.111 In particular, both a decrease in energy production and a switch in energy substrate use that occur with remodelling can worsen heart failure.111, 112
The progression of heart failure is associated with compromised myocardial energy production indicated by decreased concentrations of both ATP and phosphocreatine.113, 114 This depletion seems to result primarily from
Summary
Remodelling of the heart and vessels characterises coronary artery disease, hypertension, and heart failure. Remodelling of the coronary arteries starts in the endothelium and progressively advances towards the atherosclerotic plaque that when causing ischaemia and infarction provokes myocardial remodelling. The arteriolar microvascular response to hypertension, luminal narrowing, smooth muscle hyperplasia, and medial thickening perpetuates raised blood pressure that predisposes to myocardial
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