Alterations of hemodynamics and myocardial mechanics in patients with congestive heart failure: pathophysiologic mechanisms and assessment of cardiac function and ventricular contractility.
TL;DR: This work begins with consideration of the principal determinants governing the performance of the intact ventricle and progresses to interpretation of the experimental data which form the basis for the conclusion that, of these major determinants, the fundamental abnormality in congestive heart failure is found.
About: This article is published in Progress in Cardiovascular Diseases.The article was published on 1970-05-01. It has received 83 citations till now. The article focuses on the topics: Heart failure.
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TL;DR: It is demonstrated that the plasma norepinephrine concentration is directly related to the degree of left ventricular dysfunction in patients with congestive heart failure and suggested that beta adrenergic receptors are desensitized in these patients and that this desensitization contributes to the observed alterations in myocardial contractility.
Abstract: Resting plasma concentrations of norepinephrine, dopamine-beta-hydroxylase enzyme activity and peripheral blood lymphocyte beta adrenergic receptor sensitivity to isoproterenol as reflected in cyclic 3′,5′-adenosine monophosphate (cAMP) generation were studied in patients with congestive heart failure due to atherosclerotic heart disease or to congestive cardiomyopathy or hypertensive cardiovascular disease. Systolic time Intervals were also measured in nonhypertensive patients and correlated with the plasma norepinephrine concentration. Control patients were hospital employees without a previous history of heart disease or hypertension, and were matched for age to eliminate the effect of increasing age on the plasma norepinephrine concentration. The results of this study clearly demonstrate that the plasma norepinephrine concentration is directly related to the degree of left ventricular dysfunction in patients with congestive heart failure. When the systolic time intervals were correlated with the plasma norepinephrine levels, a significant prolongation of the preejection period was observed with progressively increasing plasma concentrations of norepinephrine. The reverse was true for the left ventricular ejection time, which demonstrated a significant Inverse relation with the plasma norepinephrine concentration. The ratio of the preejection period to the left ventricular ejection time, which is a reflection of left ventricular function, significantly increased with increasing levels of plasma norepinephrine. In addition, plasma lymphocytes from patients with the greatest degree of left ventricular dysfunction failed to generate normal amounts of cAMP after beta adrenergic receptor stimulation with isoproterenol. It Is suggested that beta adrenergic receptors are desensitized in these patients and that this desensitization contributes to the observed alterations in myocardial contractility.
896 citations
TL;DR: Changes in the respective roles of the L-type Ca2+ current, SR Ca 2+ uptake, storage and release, Ca2+, transport via the Na+-Ca2+ exchanger (NCX), and Ca2- buffering in the altered Ca2 + transients of failing human ventricular myocytes can explain the defective Ca2+.
Abstract: Depressed contractility is a central feature of the failing human heart and has been attributed to altered [Ca2+]i. This study examined the respective roles of the L-type Ca2+ current (ICa), SR Ca2+ uptake, storage and release, Ca2+ transport via the Na+-Ca2+ exchanger (NCX), and Ca2+ buffering in the altered Ca2+ transients of failing human ventricular myocytes. Electrophysiological techniques were used to measure and control V(m) and measure I(m), respectively, and Fluo-3 was used to measure [Ca2+]i in myocytes from nonfailing (NF) and failing (F) human hearts. Ca2+ transients from F myocytes were significantly smaller and decayed more slowly than those from NF hearts. Ca2+ uptake rates by the SR and the amount of Ca2+ stored in the SR were significantly reduced in F myocytes. There were no significant changes in the rate of Ca2+ removal from F myocytes by the NCX, in the density of NCX current as a function of [Ca2+]i, ICa density, or cellular Ca2+ buffering. However, Ca2+ influx during the late portions of the action potential seems able to elevate [Ca2+]i in F but not in NF myocytes. A reduction in the rate of net Ca2+ uptake by the SR slows the decay of the Ca2+ transient and reduces SR Ca2+ stores. This leads to reduced SR Ca2+ release, which induces additional Ca2+ influx during the plateau phase of the action potential, further slowing the decay of the Ca2+ transient. These changes can explain the defective Ca2+ transients of the failing human ventricular myocyte.
472 citations
Cites background from "Alterations of hemodynamics and myo..."
...myocytes when the AP wave shape is identical in NF and F; (2) under these conditions, there is reduced SR Ca(2) content and rate of SR Ca(2) uptake in F versus NF myocytes; (3) Ca(2) buffering, fractional SR Ca(2) release, and ICa,L density are unchanged in F myocytes; (4) the [Ca(2) ] dependence of INCX is unchanged in F myocytes but the contribution of NCX to Ca(2) removal is increased; (5) the slower rate of decay of the Ca(2) transient during the AP in F myocytes is caused by decreased SR Ca(2) transport and possibly changes in NCX...
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TL;DR: CPAP administered by face mask improves gas exchange, decreases respiratory work, unloads circulatory stress, and may reduce the need for ventilator treatment in acute cardiogenic pulmonary edema.
Abstract: The therapeutic efficacy of continuous positive airway pressure (CPAP) administered by face mask was studied in 40 patients with acute cardiogenic pulmonary edema and respiratory failure. Arterial blood gas values and pH, systemic arterial pressure, heart rate and respiratory rate were measured during administration of 30% oxygen with a high-flow face mask apparatus at ambient airway pressure. Twenty patients were then randomly chosen to continue ambient airway pressure breathing and 20 received 10 cm H2O of CPAP. The measurements were repeated 10, 60 and 180 minutes after therapy was initiated. During the first 10 minutes of CPAP treatment, arterial blood oxygen partial pressure increased 8 +/- 9 mm Hg (mean +/- 1 standard deviation), (p less than 0.01) and respiratory rate decreased 5 +/- 5 breaths/min (p less than 0.001). Systolic arterial pressure decreased 12 +/- 21 mm Hg (p less than 0.05), and heart rate by 10 +/- 11 beats/min (p less than 0.001). A decrease in respiratory rate by 2 +/- 5 breaths/min (p less than 0.05) was the only change that occurred in the control group. The improvement in arterial blood oxygenation persisted throughout the investigation period (p less than 0.05). Thirteen patients (65%) in the control group and 7 patients (35%) in the CPAP group met our criteria for treatment failure during the study (p = 0.068). Thus, CPAP administered by face mask improves gas exchange, decreases respiratory work, unloads circulatory stress, and may reduce the need for ventilator treatment in acute cardiogenic pulmonary edema.
347 citations
TL;DR: Although study size was not large enough to demonstrate a difference in mortality, CPAP therapy resulted in physiologic cardiovascular and pulmonary function improvement and significantly reduced the need for intubation; however, it did not decrease mortality in patients with acute cardiogenic pulmonary edema.
305 citations
TL;DR: In chronically treated heart failure patients with full angiotensin-converting enzyme-inhibition and diuretics, there is decreased compliance of the aorta and its major branches, which is inversely correlated with the aldosterone escape phenomenon.
Abstract: Aims The purpose of this study was to examine, in chronically treated heart failure patients vs control subjects, the influence of neurohumoral activation and aldosterone escape on arterial elastic behaviour, assessed by noninvasive mathematical lumped-parameter modelling of the compliance of the arterial system.
Methods and Results Radial arterial pulse waves were recorded non-invasively for 30 s with an arterial tonometer sensor array in 13 chronic heart failure patients (mean age, 59 +/- 2.5 years) in New York Heart Association class II. The patients had been taking digoxin, furosemide, captopril and aspirin for more than 3 months. Thirteen healthy subjects (mean age, 50 +/- 4.0 years) acted as controls. Compliance of the proximal (aorta and major branches, C1) and distal parts (C2) of the circulation were derived from a third order four-element modified Windkessel model which can reproduce arterial pressure waveforms, including both exponential and oscillatory sections. Active renin, angiotensin II and aldosterone levels were determined on venous blood samples in the supine position and after 30 min active standing. There was decreased proximal (C1, 1.51 +/- 0.11 ml . mmHg(-1), P<0.01) and distal (C2, 0050+/-0.011 ml . mmHg(-1)) arterial compliance in the chronic heart failure patients vs controls (C1, 1.71 +/- 0.16 ml. mmHg(-1); C2, 0.054 +/- 0.006 ml . mmHg(-1)). The chronic heart failure patients were characterized by an aldosterone escape phenomenon which was inversely correlated with the proximal arterial compliance in both supine (r= -0.795, P=0.002) and standing (r= -0.628, P=0.029) positions.
Conclusions In chronically treated heart failure patients with full angiotensin-converting enzyme-inhibition and diuretics, there is decreased compliance of the aorta and its major branches, which is inversely correlated with the aldosterone escape phenomenon.
191 citations
References
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TL;DR: In this article, a more accurate and rapid technique for muscle heat measurement was proposed, and some astonishingly simple and accurate relations have been found, which determine the effect of load on speed of shortening, allow the form of the isometric contraction to be predicted, and are the basis of the so-called "visco-elasticity" of skeletal muscle.
Abstract: The hope was recently expressed (Hill 1937, p. 116) that with the development of a more accurate and rapid technique for muscle heat measurement, a much more consistent picture might emerge of the energy relations of muscles shortening (or lengthening) and doing positive (or negative) work. This hope has been realized, and some astonishingly simple and accurate relations have been found, relations, moreover, which (among other things) determine the effect of load on speed of shortening, allow the form of the isometric contraction to be predicted, and are the basis of the so-called “visco-elasticity” of skeletal muscle. This paper is divided into three parts. In Part I further developments of the technique are described: everything has depended on the technique, so no apology is needed for a rather full description of it and of the precautions necessary. In Part II the results themselves are described and discussed. In Part III the “visco-elastic” properties of active muscle are shown to be a consequence of the properties described in Part II.
4,672 citations
TL;DR: It is postulated that a defect in the mechanical performance of the heart is responsible for the abnormal systolic time intervals in human heart failure.
Abstract: The duration of the systolic time intervals in nondigitalized patients with heart failure was determined from simultaneous fast speed recordings of the electrocardiogram, phonocardiogram, and carotid arterial pulsation. These were compared with the systolic time intervals corrected for heart rate and sex in 211 normal subjects. The failing left ventricle is characterized by a prolongation in the systolic pre-ejection period and a diminution in the left ventricular ejection time while total electromechanical systole remains relatively unaltered. Both components of the pre-ejection period, the Q-1 interval and the isovolumic contraction time, were prolonged. These alterations in the phases of systole occur in the absence of a measurable change in ventricular depolarization time. The prolongation in the pre-ejection period is well correlated with the reduced stroke volume and cardiac output in heart failure and is independently augmented by high levels of arterial pressure. The abbreviation in left ventricul...
1,272 citations
TL;DR: The possible role of the inappropriate release of antidiuretic hormone in all these disorders and in the hyponatremia which can occur postoperatively or in congestive heart failure or cirrhosis, requires further definition by new, specific assay technics.
1,126 citations
TL;DR: Pressure-volu ne relations of the diastolic left ventricle have been determined in 176 patients and demonstrate large patient-to-patient differences of ventricular distensibility in patients with different types and durations of heart disease.
Abstract: The various methods currently being used to determine left ventricular chamber volumes from biplane angiocardiograms are described and discussed. The spatial direction and change of direction and length of the long axis of the left ventricle over the heart cycle is described. The long axis of the left ventricle is in most subjects directed approximately 20 degrees from being parallel with the frontal plane of the body and results in only slight foreshortening of the long axis of the left ventricle on films taken in the anteroposterior projection. A method is described and evaluated for determining left ventricular chamber volume from angiocardiograms taken in a single anteroposterior projection. Values for normal end-diastolic volume and systolic ejection fraction obtained by various investigators using the radiographic methods are given. The application of these radiographic methods to estimate aortic and mitral valve regurgitant flow is reviewed. Pressure-volu ne relations of the diastolic left ventricle have been determined in 176 patients and demonstrate large patient-to-patient differences of ventricular distensibility in patients with different types and durations of heart disease. Measurement of compliance of the diastolic left ventricle from the pressure-volume curves is discussed. By relating pressure and volume curves over the entire heart cycle, left ventricular pressure-volume curves can be constructed and from these the various components of pressure-volume work determined: systolic work, work done in distending the ventricle during diastole, and net work. Values obtained for these various components of ventricular work in patients with heart and valvular disease are discussed. A method for calculating wall tension and stress from measurement of chamber pressure and chamber dimensions is reviewed. Left ventricular mass can be calculated from chamber dimensions and wall thickness determined from angiocardiograms. A value of 92 ± 16 gm. has been obtained by this method in patients without left ventricular disease, and this is similar to values obtained in earlier postmortem studies. Measurement of left ventricular oxygen consumption and mechanical efficiency in patients with heart disease is discussed.
641 citations
TL;DR: The pattern of left ventricular contraction is described as a "series of sequential fractionate contractions of muscle bundles" and the possibility that unco-ordinated contraction of the heart results from a combination of normal and abnormal muscle has received little attention.
Abstract: CONGESTIVE heart failure has usually been considered to be a global affection of the myocardium in which disturbance of contraction in one or both ventricles is generalized. On the other hand, abnormal myocardial contraction may be caused by local areas of malfunctioning myocardium interacting with other areas of completely normal muscle. The possibility that unco-ordinated contraction of the heart results from such a combination of normal and abnormal muscle has received little attention. In 1925 Wiggers1 described the pattern of left ventricular contraction as a "series of sequential fractionate contractions of muscle bundles." He suggested that disturbance in this temporal . . .
634 citations