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Left Ventricular Hypertrophy, Cardiac Diseases and Hypertension: Recent Experiences

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Left Ventricular Hypertrophy, Cardiac Diseases and Hypertension: Recent Experiences View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector JACC Vol. 14, No. 7 1587 December 1989: 1587-93 --- ACC ANNIVERSARY SEMINAR Suzanne B. Knoebel, MD, FACC, Guest Editor Left Ventricular Hypertrophy, Cardiac Diseases and Hypertension: Recent Experiences EDWARD D. FROHLICH, MD, FACC New Orleans. Louisiana -- Heart disease in the patient with hypertension is many- Borderline or mild essential hypertension. This hyperdy- faceted (l-4). It may be an adaptive response to sustained namic circulation associated with hypertensive disease may and protracted pressure overload or it may coexist with an have various expressions. One common manifestation is associated disease. It may vary according to the severity of frequently found in patients with borderline (labile) or mild the hypertensive vascular disease, the complex- essential hypertension. In these patients, an :kl : e: .e: ity of the pathophysiologic mechanisms in- elevated cardiac output, faster heart rate and volved or the coexisting problems offered by one . j . increased myocardial contractility may be the or more associated diseases. As a result, the - - pathophysiologic manifestations of early disease management of cardiac disease in the patient that involve the same pressor mechanism. In the with hypertension is dependent on the nature early stage of the disease this may appear to be and extent of cardiac involvement and the the result of increased adrenergic input to the pathophysiologic mechanisms involved. heart, arterioles and venules. but these changes This renort provides a review of the variabil- A N N ’ ” E R ’ A R ’ may also reflect interactions with the renopres- ity and extent of the functional involvement of ’ ’ 4 ’ 1 9 8 9 sor or other pressor or modulating systems (1,2). the heart in hypertension. It is written with a plea to the Moreover, the elevated cardiac output is not secondary to an student, practitioner and investigator of this major clinical expanded intravascular (plasma) volume: in fact, plasma problem to consider it apart from other diseases associated volume is usually normal or contracted (7,11,12). However, with pressure overload of the left ventricle. The pathogene- the increased output results from peripheral venoconstric- sis, the involved pathophysiologic mechanisms, the rate of tion that redistributes the circulating intravascular volume development of cardiac involvement and other aspects of centrally to the cardiopulmonary area, thereby increasing hypertensive heart disease are different from those of other venous return (13). Furthermore if autonomic input to the conditions associated with pressure overload (4-6). heart is inhibited pharmacologically with parasympathetic (i.e., atropine) and beta-adrenergic receptor (i.e., pro- pranolol) blocking agents, the elevated cardiac output is Hyperdynamic Heart equilibrated with that of normotensive individuals who are Early in the development of hypertensive heart disease, similarly treated (14,15), thereby demonstrating that the cardiac involvement may be manifested by findings associ- so-called normal total peripheral resistance in the untreated ated with a hyperdynamic circulation (4,7-9). These may individual was “inappropriately normal” and actually in- include a faster heart rate, greater cardiac output than creased (7-9). normal, an increased myocardial contractility with increased oxygen consumption and, perhaps, increased circulating catecholamines or responsiveness of the myocardial and This article is part of a series of articles celebrating the vascular beta-adrenergic receptor sites (610). 40th anniversary of the American College of Cardiology. The series attempts to set the stage for the future by describing current state of the art management of selected From the Alton Ochsner Medical Foundation, New Orleans. Louisiana. major cardiovascular problems and the basic knowledge Address for reorints: Edward D. Frohlich. MD. Vice President for Academic Affairs, Alton Ochsner Medical Foundation, 1516 Jefferson High- that will provide directions for advances in diagnosis and way, New Orleans, Louisiana 70121. therapy. 01989 by the Amencan College of Cardiology 0735.1097189/$3.50 1588 FROHLICH JACC Vol. 14, No. 7 CARDIAC DISEASES AND HYPERTENSION December 1989:1587-94 Thus, this hyperdynamic state is one of a net increase in circulation, elevated levels of circulating catecholamines adrenergic input to the cardiovascular system, and it still is (not as high as those levels associated with pheochromo- not known whether this results from increased sympathetic cytoma), increased responsiveness of myocardial beta- outflow from the brain, hyperresponsiveness of beta- adrenergic receptor sites and aggravation of the mitral valve adrenergic receptor sites, increases in circulating levels of prolapse during isoproterenol infusion (21,22). Reversal of catecholamines, adrenergic “drive” mediated by the periph- the findings and improvement of the prolapsed valve may be erally circulating or centrally active renopressure system or expected with beta-blocker therapy. other mechanisms (16). Thus, these alterations constitute a hyperdynamic heart “Hyper-beta state.” Another segment of patients with syndrome and patients with these changes may be treated hyperdynamic circulation comprises those patients with a best with beta-adrenergic receptor blocking drugs. How- hyperdynamic beta-adrenergic circulatory state (17,18). ever, if a beta-blocker cannot be prescribed, calcium antag- These patients present clinically with variable cardiovascu- onists, adrenergic inhibitors and angiotensin-converting en- lar manifestations that reflect increased adrenergic input to zyme (ACE) inhibitors may be used, although clinical the heart and vessels. Thus, in contrast to the foregoing improvement may not be as clear-cut as with the beta- group of asymptomatic patients with borderline (labile) or blocking agents. mild to moderate essential hypertension, these patients have complaints related to excess stimulation of myocardial or vascular smooth muscle beta-adrenergic receptor sites. Left Ventricular Hypertrophy These symptoms include a more forceful or rapid heart rate, Hemodynamic factors. As hypertension becomes well ectopic cardiac (atria1 or ventricular) beats, palpitation in the established in patients with essential hypertension, arterial rest or reflexively stimulated (e.g., upright posture or exer- pressure rises pari passu with the increasing total peripheral cise) state or feelings of flushing, hot flashes, weakness or resistance, the classic hemodynamic hallmark of hyperten- faintness. Physically, the findings may be manifested by sion (8,9,23). This increased pressure overload imposed on systolic or systolic and diastolic pressure elevation, faster the left ventricle results in a structural hypertrophic adapta- heart rate, systolic ejection type murmur, cardiac dysrhyth- tion that is generally concentric in nature (24,25). The mias and flushing (often in the facial or neck and upper development of left ventricular hypertrophy, however, may thoracic areas). The findings in earlier years prompted such not be totally explained by hemodynamic pressure overload diagnoses as irritable heart, soldier’s heart, effort syndrome, (l-4,26,27). Some patients with hypertension may also have hyperkinetic heart syndrome or neurocirculatory asthma a component of volume overload imposed on the left ventri- (19,20). cle by various factors including physiologic volume overload Physiologic&&zgs include a hyperkinetic circulation, as associated with prolonged exercise; pathologically induced outlined previously, slight elevation of circulating catechol- volume overload associated with either volume-dependent amines (not as high as levels associated with those in essential hypertension or other forms of volume-dependent patients having pheochromocytoma) and increased respon- secondary forms of hypertension (e.g., renal parenchymal siveness of myocardial beta-adrenergic receptor sites to disease, steroidal hypertension, primary aldosteronism or infusion of the synthetic beta-adrenergic receptor agonist congestive heart failure) or exogenous obesity (3,4,28-30). isoproterenol. In fact, intravenous infusion of isoproterenol Nonbemodynamic factors. Still another very important will provoke the symptoms experienced by these patients and exciting new aspect of the development of left ventric- when they are active or assume upright posture (17,18). ular hypertrophy relates to specific “nonhemodynamic” These symptoms may include anxiety attack, hysteric out- factors that have been clinically and experimentally associ- bursts and accentuation of milder symptoms that would ated with the development of left ventricular hypertrophy ordinarily be associated with beta-adrenergic receptor stim- (26,27). These findings are supported by clinical observa- ulation. Moreover, after intravenous administration of a tions that indicate that height of arterial pressure in itself beta-adrenergic blocking agent (e.g., propranolol) these may not be correlated totally with developed left ventricular physiologic and clinical findings will be normalized or pre- mass or wall thickness. In part, this may be because the vented. pressures obtained to relate with mass and wall thickness do Mitral valve prolapse. A third manifestation of a hyper- not reflect the integrated arterial pressures actually occur- dynamic circulation may be seen in patients with idiopathic ring throughout the
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