Effectiveness of preload reserve as a determinant of clinical status in patients with left ventricular systolic dysfunction

Konstam, Marvin A.; Kronenberg, Marvin W.; Udelson, James E.; Kinan, Debra; Metherall, Jeanne; Dolan, Noreen; Edens, Tonya R.; Howe, Donna; Kilcoyne, Lori; Benedict, Claude R.; Youngblood, Marston; Barrett, Joan; Yusuf, Salim

doi:10.1016/0002-9149(92)90709-8

Cited by 32 publications

(5 citation statements)

References 27 publications

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“…This study may also demonstrate that the concept of preload reserve used most commonly in reference to ischemic heart disease associated limitations in cardiac performance may also apply to septic shock [ 32 ]. Several groups of investigators have shown that subjects with clinically asymptomatic impairment of systolic cardiac function can be differentiated from symptomatic patients by the presence of exercise stress-induced increases in SVI in association with ventricular dilatation [ 33 , 34 ]. No direct link has yet been made between survival and the presence of this phenomenon among patients with impaired heart function.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular response to dobutamine stress predicts outcome in severe sepsis and septic shock

Kumar

Schupp²,

Bunnell³

et al. 2008

Crit Care

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Introduction During septic shock, resistance to the haemodynamic effects of catecholamine vasopressors and inotropes is a well-recognised marker of mortality risk. However, the specific cardiovascular or metabolic response elements that are most closely associated with outcome have not been well defined. The objective of this study was to assess cardiovascular and metabolic responses to dobutamine as correlates of outcome in patients with severe sepsis or septic shock.

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Section: Discussionmentioning

confidence: 99%

Cardiovascular response to dobutamine stress predicts outcome in severe sepsis and septic shock

Kumar

Schupp²,

Bunnell³

et al. 2008

Crit Care

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“…This differs from the indirect plasma volume determination, which cannot localize the plasma volume. The radionuclide technique has been validated and used successfully in many studies to determine left ventricular filling and function (16,20,21). The advantage of this technique over echocardiography or angiography is that it is based on the total radioactive count in the entire ventricle, without resorting to frequently invalid geometric assumptions.…”

Section: Discussionmentioning

confidence: 99%

Central blood volume in cirrhosis: Measurement by radionuclide angiography

WONG¹

1993

Hepatology

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In patients with cirrhosis a diminished effective central arterial blood volume associated with systemic arterial vasodilatation has been proposed as the mechanism that initiates renal sodium retention. Furthermore, total central blood volume has recently been reported as reduced in cirrhosis, and the controversy over the stimulus for sodium retention in cirrhosis remains. The aim of this study was to assess the central blood volume with radionuclide angiography to determine whether there is effective arterial underfilling in cirrhosis. Twenty-nine patients (13 with and 16 without ascites) and 10 age-and sex-matched control subjects were studied under metabolic conditions. Radionuclide ventricular volume and total central blood volume were determined from gated images, taking into account the ssTc count activity per milliliter of blood volume and attenuation. The pulmonary volumes were similarly derived. The cirrhotic patients as a group had significantly higher total central blood volume (1,287 & 105 ml/m2 in control subjects vs. 1,874 * 106 ml/m2 in cirrhotic patients, p < 0.01), right and left pulmonary blood volumes (217 f 20 ml/m2 in control subjects vs. 309 2 20 ml/m2 in cirrhotic patients, p = 0.03 and 185 * 18 ml/m2 in control subjects vs 288 k 22 ml/m2 in cirrhotic patients, p = 0.02, respectively), cardiac and central vascular blood volume (885 & 79 ml/m2 in control subjects vs. 1,276 * 75 ml/m2 in cirrhotic patients, p = 0.01), cardiac output (5.36 2 0.56 L/min in control subjects vs. 7.19 * 0.50 L/min in cirrhotic patients, p = 0.05), heart rate (65 2 3 beats/min in control subjects vs. 75 f 2 beats/min in cirrhotic patients, p = 0.04) and significantly lower systemic vascular resistance (1,443 2 121 dyne sec * cm-5 in control subjects vs. 1084 * 68 dyne sec .in cirrhotic patients, p = 0.02). All volumes were significantly higher in both the nonascitic and the ascitic patients when compared with the control subjects. Significantly increased cardiac output and reduced systemic vascular resistance,

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“…36 Both the echocardiography substudy 37 and the radionuclide ventriculography and catheterization substudy 38 showed significant differences in change of left ventricular volumes during serial measurements between active treatment and placebo groups (P = 0.025 and P = 0.008 for EDV and P = 0.019 and P = 0.002 for ESV, respectively). However, while Konstam et al observed significant reductions in EDV (140 ± 44 to 127 ± 37 mL/m 2 , P = 0.02) and ESV (106 ± 42 to 93 ± 37 mL/m 2 , P = 0.01), as well as an increase in LVEF (25 ± 7% to 29.8%, P = 0.01) after 1 year study period, 38 no significant change in the aforementioned parameters was seen in the echo substudy. 37 Also, no change in EDV was observed after 12 months of treatment with captopril in a small, single-centre RCT of 50 patients followed up by echocardiography.…”

Section: Renin-angiotensin-aldosterone Inhibitionmentioning

confidence: 96%

Left ventricular reverse remodelling and its predictors in non‐ischaemic cardiomyopathy

2022

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Adverse remodelling following an initial insult is the hallmark of heart failure (HF) development and progression. It is manifested as changes in size, shape, and function of the myocardium. While cardiac remodelling may be compensatory in the short term, further neurohumoral activation and haemodynamic overload drive this deleterious process that is associated with impaired prognosis. However, in some patients, the changes may be reversed. Left ventricular reverse remodelling (LVRR) is characterized as a decrease in chamber volume and normalization of shape associated with improvement in both systolic and diastolic function. LVRR might occur spontaneously or more often in response to therapeutic interventions that either remove the initial stressor or alleviate some of the mechanisms that contribute to further deterioration of the failing heart. Although the process of LVRR in patients with new-onset HF may take up to 2 years after initiating treatment, there is a significant portion of patients who do not improve despite optimal therapy, which has serious clinical implications when considering treatment escalation towards more aggressive options. On the contrary, in patients that achieve delayed improvement in cardiac function and architecture, waiting might avoid untimely implantable cardioverter-defibrillator implantation. Therefore, prognostication of successful LVRR based on clinical, imaging, and biomarker predictors is of utmost importance. LVRR has a positive impact on prognosis. However, reverse remodelled hearts continue to have abnormal features. In fact, most of the molecular, cellular, interstitial, and genome expression abnormalities remain and a susceptibility to dysfunction redevelopment under biomechanical stress persists in most patients. Hence, a distinction should be made between reverse remodelling and true myocardial recovery. In this comprehensive review, current evidence on LVRR, its predictors, and implications on prognostication, with a specific focus on HF patients with non-ischaemic cardiomyopathy, as well as on novel drugs, is presented.

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Effectiveness of preload reserve as a determinant of clinical status in patients with left ventricular systolic dysfunction

Cited by 32 publications

References 27 publications

Cardiovascular response to dobutamine stress predicts outcome in severe sepsis and septic shock

Cardiovascular response to dobutamine stress predicts outcome in severe sepsis and septic shock

Central blood volume in cirrhosis: Measurement by radionuclide angiography

Left ventricular reverse remodelling and its predictors in non‐ischaemic cardiomyopathy

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