Doppler-derived mitral deceleration time of early filling as a strong predictor of pulmonary capillary wedge pressure in postinfarction patients with left ventricular systolic dysfunction

Giannuzzi, Pantaleo; Imparato, Alessandro; Temporelli, Pier Luigi; Vito, Francesco; Silva, Pedro L.; Scapellato, Francesco; Giordano, Amerigo

doi:10.1016/0735-1097(94)90667-x

Cited by 348 publications

(168 citation statements)

References 26 publications

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“…Increased E-wave velocity and decreased peak A-wave velocity (or absent A wave), resulting in greater E/A ratios, and decrease of DcT of E waves were observed in our MI rats, and these flow patterns were similar to transmitral flow profiles observed in patients with heart failure with restrictive patterns (8,21) and in an experimental large MI model in rats (26). In this study, treatment with IMD significantly decreased the E/A ratio and improved the DcT, indicating amelioration of diastolic dysfunction.…”

Section: Diastolic Dysfunction and Nf-b Inhibitionsupporting

confidence: 51%

Inhibition of NF-κB improves left ventricular remodeling and cardiac dysfunction after myocardial infarction

Onai¹,

Suzuki²,

Maejima³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

109

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August 18, 2006; doi:10.1152/ajpheart.00549.2006.-Several studies have demonstrated that NF-B is substantially involved in the progression of cardiac remodeling; however, it remains uncertain whether the continuous inhibition of NF-B is effective for the prevention of myocardial remodeling. Myocardial infarction (MI) was produced by ligation of the left anterior coronary artery of rats. IMD-0354 (10 mg/kg per day), a novel phosphorylation inhibitor of I B that acts via inhibition of IKK-␤, was injected intraperitoneally starting 24 h after induction of MI for 28 days. After 28 days, the IMD-0354-treated group showed significantly improved survival rate compared with that of the vehicle-treated group (P Ͻ 0.05). Although infarct size was similar in both groups, improved left ventricular (LV) remodeling and diastolic dysfunction, as indicated by smaller LV cavity (LV enddiastolic area: vehicle, 74.13 Ϯ 3.57 mm 2 ; IMD-0354, 55.00 Ϯ 3.73 mm 2 ; P Ͻ 0.05), smaller peak velocity of early-to-late filling wave (E/A) ratio (vehicle, 3.87 Ϯ 0.26; IMD-0354, 2.61 Ϯ 0.24; P Ͻ 0.05), and lower plasma brain natriuretic peptide level (vehicle, 167.63 Ϯ 14.87 pg/ml; IMD-0354, 110.75 Ϯ 6.41 pg/ml; P Ͻ 0.05), were observed in the IMD-0354-treated group. Moreover, fibrosis, accumulation of macrophages, and expression of several factors (transforming growth factor-␤1, monocyte chemoattractant protein-1, matrix metalloproteinase-9 and -2) in the noninfarcted myocardium was remarkably inhibited by IMD-0354. In conclusion, inhibition of NF-B activation may reduce the proinflammatory reactions and modulate the extracellular matrix and provide an effective approach to prevent adverse cardiac remodeling after MI. experimental heart failure; nuclear factor-b; matrix metalloproteinase; echocardiography MYOCARDIAL INFARCTION (MI) frequently leads to left ventricular (LV) dilatation and associated interstitial fibrosis in the noninfarcted myocardium. This adverse LV remodeling causes depressed cardiac performance and is an independent determinant of morbidity and mortality after MI (20). One of the recent conceptual advances in our understanding of the pathogenesis of LV remodeling is that this process is driven by the overexpression of various factors, including proinflammatory cytokines, angiotensin II, and norepinephrine, which have direct pathophysiological effects on cardiac myocytes, noncardiac myocytes, and the extracellular matrix (20). Although the expression of proinflammatory cytokines may be involved in wound healing after MI, it is believed that the overexpression of cytokines damages cardiac tissue and evokes excess deposition of fibrotic components, even in the noninfarcted myocardium.Several recent studies reported that nuclear factor-B (NF-B) is involved in the pathogenesis of heart failure (7, 35). Activation of NF-B induces activation of genetic programs that lead to transactivation of cytokines, chemokines, and matrix metalloproteinases (MMPs), promoting inflammatory and fibrotic responses that participate in the progre...

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Section: Diastolic Dysfunction and Nf-b Inhibitionsupporting

confidence: 51%

Inhibition of NF-κB improves left ventricular remodeling and cardiac dysfunction after myocardial infarction

Onai¹,

Suzuki²,

Maejima³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

109

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“…In patients with overt heart failure, CSA correlated with pulmonary capillary wedge pressure, as measured by invasive 22 and noninvasive 23,24 approaches. In our present study of patients with LV dysfunction without overt heart failure, the presence and severity of CSA was not associated with increased ventricular impairment or hemodynamic indices of increased filling pressure (Figure 2).…”

Section: Discussionmentioning

confidence: 99%

Central Sleep Apnea in Left Ventricular Dysfunction

et al. 2003

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Background— The prevalence and characteristics of sleep-disordered breathing in patients with asymptomatic left ventricular (LV) dysfunction are unknown. Therefore, we evaluated the prevalence of sleep-disordered breathing in patients with LV dysfunction without overt heart failure and tested the hypothesis that sleep-disordered breathing is linked to greater hemodynamic and autonomic impairment. Methods and Results— We studied 47 patients with LV ejection fractions ≤40% without any history of heart failure. Central sleep apnea (CSA), as defined by an apnea-hypopnea index ≥15/h, was present in 26 patients (55%), 17 (36%) of whom had severe CSA (apnea-hypopnea index ≥30/h). Obstructive sleep apnea was evident in 5 patients (11%). The prevalence and severity of CSA were higher in patients with ischemic cardiomyopathy than in patients with nonischemic cardiomyopathy ( P <0.05). Exercise tolerance and echocardiographic indices of systolic and diastolic function were similar in patients without CSA, with mild CSA, and with severe CSA. Heart rate variability was markedly depressed in patients with CSA ( P <0.05). Patients with severe CSA also had a higher incidence of nonsustained ventricular tachycardia ( P =0.05). Conclusions— CSA is highly prevalent in patients with asymptomatic LV dysfunction. The severity of CSA may not be related to the severity of hemodynamic impairment. Severe CSA is associated with impaired cardiac autonomic control and with increased cardiac arrhythmias.

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“…The diagnosis is usually made with the help of pulmonary artery (PA) catheterization; however, Doppler echocardiography may also be used to confirm elevation of LV filling pressures. 1 Hypoperfusion may be manifest clinically by cool extremities, decreased urine output, and/or alteration in mental status. Hemodynamic abnormalities form a spectrum that ranges from mild hypoperfusion to profound shock, and the short-term outcome is directly related to the severity of hemodynamic derangement.…”

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confidence: 99%

Cardiogenic Shock

2008

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ardiogenic shock (CS) occurs in Ϸ5% to 8% of patients hospitalized with ST-elevation myocardial infarction (STEMI). Recent research has suggested that the peripheral vasculature and neurohormonal and cytokine systems play a role in the pathogenesis and persistence of CS. Early revascularization for CS improves survival substantially. New mechanical approaches to treatment are available, and clinical trials are feasible even in this high-risk population. Most importantly, hospital survivors have an excellent chance for long-term survival with good quality of life. This review will outline the causes, pathophysiology, and treatment of CS with a focus on CS complicating myocardial infarction (MI.) The case will be made for viewing CS as a serious disorder with a high early death rate, but one that is treatable and that, if approached aggressively, can result in full recovery. The diagnosis is usually made with the help of pulmonary artery (PA) catheterization; however, Doppler echocardiography may also be used to confirm elevation of LV filling pressures. 1 Hypoperfusion may be manifest clinically by cool extremities, decreased urine output, and/or alteration in mental status. Hemodynamic abnormalities form a spectrum that ranges from mild hypoperfusion to profound shock, and the short-term outcome is directly related to the severity of hemodynamic derangement. MI with LV failure remains the most common cause of CS. It is critical to exclude complicating factors that may cause shock in MI patients. Chief among these are the mechanical complications: ventricular septal rupture, contained free wall rupture, and papillary muscle rupture. Mechanical complications must be strongly suspected in patients with CS complicating nonanterior MI, particularly a first MI. Echocardiography is the technique of choice to rule out these entities and should be performed early unless the diagnosis is extensive anterior MI and the patient is undergoing prompt percutaneous coronary intervention (PCI). In addition, the detection of valvular disease before angiography may alter the revascularization approach. Diagnosis and CausesHemorrhage, infection, and/or bowel ischemia may contribute to shock in the setting of MI. As with mechanical complications, a high index of suspicion is required to make these diagnoses in MI patients, and survival may depend on timely recognition and treatment.Any cause of acute, severe LV or RV dysfunction may lead to CS. Acute myopericarditis, tako-tsubo cardiomyopathy, and hypertrophic cardiomyopathy may all present with ST elevation, release of cardiac markers, and shock in the absence of significant coronary artery disease. Stress-induced cardiomyopathy, also known as apical ballooning or takotsubo cardiomyopathy, is a syndrome of acute LV dysfunction after emotional or respiratory distress that leads to CS in 4.2% of cases. 2 Acute valvular regurgitation, typically caused by endocarditis or chordal rupture due to trauma or degenerative disease, may also cause CS. Aortic dissection may lead to CS via acute,...

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Doppler-derived mitral deceleration time of early filling as a strong predictor of pulmonary capillary wedge pressure in postinfarction patients with left ventricular systolic dysfunction

Abstract: Doppler-derived mitral deceleration time of early filling provides a simple and accurate means of estimating pulmonary capillary wedge pressure that is particularly useful in patients with a normal or normalized mitral flow velocity pattern.

Cited by 348 publications

References 26 publications

Inhibition of NF-κB improves left ventricular remodeling and cardiac dysfunction after myocardial infarction

Inhibition of NF-κB improves left ventricular remodeling and cardiac dysfunction after myocardial infarction

Central Sleep Apnea in Left Ventricular Dysfunction

Cardiogenic Shock

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