For example, it occurs in what is regarded as a physiologic, adaptive process in pregnancy in response to increased blood volume; but can also occur as a consequence of ventricular remodeling following a heart attack. Importantly, pathologic and physiologic remodeling engage different cellular pathways in the heart and result in different gross cardiac phenotypes. The ventricles are the chambers in the heart responsible for pumping blood either to the lungs right ventricle  or to the rest of the body left ventricle.
Concentric hypertrophy results from various stressors to the heart including hypertension, congenital heart defects such as Tetralogy of Fallot , valvular defects aortic coarction or stenosis , and primary defects of the myocardium which directly cause hypertrophy hypertrophic cardiomyopathy.
The underlying commonality in these disease states is an increase in pressures that the ventricles experience. For example, in tetralogy of Fallot, the right ventricle is exposed to the high pressures of the left heart due to a defect in the septum; as a result the right ventricle undergoes hypertrophy to compensate for these increased pressures. Similarly, in systemic hypertension, the left ventricle must work harder to overcome the higher pressures of the vascular system and responds by thickening to deal with increased wall stress.
Concentric hypertrophy is characterized by an addition of sarcomeres the contractile units of cardiac cells in parallel. The result is an increase in thickness of the myocardium without a corresponding increase in ventricular size.
This is maladaptive largely because there is not a corresponding proliferation of the vasculature supplying the myocardium, resulting in ischemic areas of the heart. Ultimately, this response can be compensatory for a duration, and allow for improved cardiac function in the face of stressors. However, this type of hypertrophy can result in a dilated ventricle which is unable to effectively pump blood, leading to heart failure. Eccentric hypertrophy is generally regarded as healthy, or physiologic hypertrophy and is often termed " athlete's heart.
It is a response to 'volume-overload', either as a result of increased blood return to the heart during exercise, or a response to an actual increase in absolute blood volume as in pregnancy. This increase in pumping ability is the result of the addition of sarcomeres in series, which enables the heart to contract with greater force.
Rowers, cyclists, and cross-country skiers tend to have the largest hearts, with an average left ventricular wall thickness of 1. Though eccentric hypertrophy is termed 'athlete's heart' it is typically only found in individuals who are aerobically conditioned. For example, weight lifters tend to undergo remodeling which more closely resembles concentric hypertrophy, as the heart does not experience a volume-overload, but instead responds to transient pressure overload as a consequence of increased vascular resistance from pressures exerted on arteries by sustained muscular contraction.
Though it is the case that eccentric hypertrophy is largely considered to be a healthy response to increased cardiac demand, it is also associated with risks.
For example, in athletes with significantly increased left ventricular weight there is also a corresponding increased risk for conduction abnormalities and sudden cardiac death. Additionally, in pregnant individuals, a subpopulation progress to peripartum cardiomyopathy , characterized by a dilation of the left ventricle and a corresponding deficit in heart function.
There are suggestions that this progression is partially determined by underlying metabolic derangement diabetes and hypertension which may result in a more maladaptive cardiac response to pregnancy. As such, though it is convenient to consider clear cut distinctions between pathologic and physiologic cardiac hypertrophy, there may be a broader range of phenotypes than may be accounted for by gross cardiac phenotypes alone. The development of pathologic states in LVH is complex. Electrical abnormalities are commonly found in individuals with LVH, both ventricular and super-ventricular tachycardia.
Regarding the procedure using aortic cross-clamping with duration inferior to minutes, both blood and crystalloid cardioplegia solutions are equivalent, especially if crystalloid cardioplegia is oxygenated . The addition of several components in some compositions to perfusate is what characterizes the blood cardioplegia, such as electrolytes, sodium bicarbonate, calcium chelating, vasodilators, and even insulin . Furthermore, a mixture in the following proportion, four parts of perfusate and one part of crystalloid solution, which is called "mother" solution, can be presented in two forms: one is more concentrated to induce electromechanical arrest of the heart, and another less concentrated for maintenance of myocardial reperfusion and cardioplegia Tables 2 to 5 .
In this kind of procedure, cardioplegia can be administered by an antegrade route, going through coronary circulation following the normal blood flow direction, applying a solution directly into the aortic root, or, selectively in both ostia of the coronary arteries, or, occasionally, into the coronary grafts. Also, it can be retrogradely delivered through the coronary sinus ostium in the right atrium, and it can go through coronary circulation into the opposite direction, being harvested in the aortic root .
Regarding to temperature, blood cardioplegia can be delivered either hypothermically, normothermically, or tepidly .
Hypothermic cardioplegia is not recommended in cases of ventricular hypertrophy, severe heart failure, significant myocardial ischemia, and cardiogenic shock, among others. This technique reduces the expenditure of high-energy phosphates as well as its production during aortic crossclamping period. However, in the abovementioned circumstances, the myocardium can already present an important metabolic deficit with a lower production of such phosphates .
The continuous tepid blood cardioplegia, described by Braile, aims at myocardial protection by delivering the cardioplegic solution by both intermittent antegrade and continuous retrograde routes. This kind of cardioplegia has shown to reduce ischemic and functional damage either reducing the increase of serum troponins [66,67] or as a lower increase of lactate  and better functional preservation .
The explanation is better understood through a better cardioplegic solution distribution, especially for regions of interventricular septum, right atrium and ventricle, including the conducting system of heart [70,71]. The concern with myocardial protection will always be one of the most important points, from the moment to decide to submit the patient to cardiac surgery on, always keeping in mind that such procedure aims at improving the patient's quality of life, especially of those who already have some degree of deficiency from cardiac muscle work. Recent studies could have evidenced a cellular cardiac metabolic activity during the induced cardiac arrest with cardioplegic solution, thus proving the need to adequately supply nutrients and oxygen.
Yet supplying adequately substrates, there is a production of free radicals, changes in transmembrane potentials, and possibility of cellular edema, being necessary to add to the cardioplegic solution not only nutrients but also free radical scavengers and membrane stabilizers , some of them with antiarrhythmic properties.
The studies have also shown the superiority of blood cardioplegia over the crystalloid cardioplegia, especially by its more physiologic characteristics. And, at last, regarding myocardial protection to a hypertrophied heart, experimental studies have shown the superiority of tepid blood cardioplegia in relation to hypothermic crystalloid, but this pathological entity, increasingly supervening in the population, constitutes an eternal challenge for cardiac surgeons, besides the intrinsically patient's characteristics.
However, we should always have in mind that the state-of-the-art was not achieved yet. Buffolo E. Rev Bras Anestesiol. Structural changes in the human myocardium following hypoxia.
J Thorac Cardiovasc Surg. Enhanced myocardial protection during ischemic arrest. Oxygenation of a crystalloid cardioplegic solution. Jatene AD. Rev Assoc Med Bras.
Fluorocarbon cardioplegia and myocardial protection. Ann Thorac Surg. Continuous warm versus intermittent cold blood cardioplegia for coronary bypass surgery in patients with left ventricular dysfunction. Eur J Cardiothorac Surg. Effect of intermittent warm blood cardioplegia on functional recovery after prolonged cardiac arrest. How to protect hypertrophied myocardium? A prospective clinical trial of three preservation techniques. Int J Artif Organs. Metabolic recovery after global myocardial ischemia: effects of blood cardioplegic solutions.
Can J Cardiol. J Extra Corpor Technol. Myocardial protection for acquired heart disease surgery: results of a national survey.
Knobel E. Condutas no paciente grave. Abduch MCD. Jessup M, Brozena S. Heart failure. N Engl J Med. Barauna VG. Experimental myocardial hypertrophy induced by a minimally invasive ascending aorta coarctation. Braz J Med Biol Res. Remodelamento ventricular: dos mecanismos moleculares e celulares ao tratamento.
Myocyte necrosis is the basis for fibrosis in renovascular hypertensive rats. Arq Bras Cardiol. Alterations in myocardial collagen content affect rat papillary muscle function. Pittella FJM. Rio de Janeiro:Editorial Laranjeiras; Rev Bras Cir Cardiovasc.
Advertisement Hide. Cardiovasc Res. Mechanical stretch was long regarded as the main trigger of myocardial remodeling. Or, to put it in simpler terms: it is an increase in cardiac muscle mass when cardiac muscle fibers thicken, or cells become enlarged, due to chronic and increased stress on the heart. Apstein CS, Taegtmeyer H. Extracellular signal-regulated kinases 1 and 2 regulate the balance between eccentric and concentric cardiac growth. Glucose transporter upregulation improves ischemic tolerance in hypertrophied failing heart.
Does cardioplegia type affect outcome and survival in patients with advanced left ventricular dysfunction? Principles of cardioplegic myocardial protection. In: Roberts AJ, editor. Myocardial protection in cardiac surgery. New York: Marcel Dekker; Capillary leakage in inflammation.
A study by vascular labeling. Am J Pathol. The addition of glucose and insulin to an oxygenated cardioplegic solution CS. J Mol Cell Cardiol. Creatine phosphate supplementation of cardioplegia: a clinical study. Rev Latinoamer Tecnol Extracorp. Acute effects of increased serum osmolality on left ventricular performance. Am J Physiol. Benefits of normothermic induction of blood cardioplegia in energy-depleted hearts, with maintenance of arrest by multidose cold blood cardioplegic infusions.
Myocardial protection with blood cardioplegia in ischemically injured hearts: reduction of reoxygenation injury with allopurinol. Rev Bras Med Esporte. Superoxide dismutase. An enzymic function for erythrocuprein hemocuprein. J Biol Chem. Pathophysiology of the hypertrophied heart in man H.