Absence Of Left Ventricular Failure Research Articles

Selection and timing for invasive therapy in non-ST-segment elevation acute coronary syndrome: Impact in the real world

The optimal timing of coronary intervention in patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACSs) is a matter of debate. We proposed through this work to study the optimal time to coronary angiography in patients admitted for NSTE-ACS and its prognostic impact on in-hospital mortality. It is about a single-center observational study that included 507 patients admitted for acute coronary syndrome without ST-segment elevation from January 2011 until December 2015. The average age of our patients was 62.85 ± 11.37 years. Nearly half of our patients (49.5%) were considered at high cardiovascular risk. The average to coronary angiography was 4.09 days. Patients who underwent early coronary angiography were significantly younger ( P = 0.01), had a lower incidence of diabetes ( P = 0.01), left heart failure ( P = 0.0001) and electrical changes suggestive of ischemia ( P = 0.0009). Patients who have undergone an invasive strategy had significantly lower levels of creatinine ( P < 0.0001) and significantly lower GRACE score ( P = 0.0001). The absence of renal failure, the absence of left ventricular failure, a low GRACE score and the absence of anemia were independent predictors of use of an invasive strategy. The overall mortality among patients included in the study was 2.9%. High heart rate ( P = 0.04), presence of heart failure ( P = 0.01), a high serum creatinine ( P < 0.001) and GRACE score ( P < 0.0001) were predictors of mortality in ACS ST (−) in our population. All cases of death were observed in the medically treated or the delayed coronary angiography group (0% vs. 2.9%, P = 0.01). The group that underwent early coronary angiography had a statistically significant reduction in MACE (3.4% vs. 15.7%, P = 0.04). Despite the fact that our work has showed that invasive strategy is associated with a better prognosis in NSTE-ACS patients, the use of this strategy remains insufficient.

0409: Selection and timing for invasive therapy in non ST segment elevation acute coronary syndrome: Impact in the real world

The optimal timing of coronary intervention in patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACSs) is a matter of debate. We proposed through this work to study the optimal time to coronary angiography in patients admitted for acute coronary syndrome without ST-segment elevation in the Tunisian context and its prognostic impact on inhospital mortality. It is about an observational study from MIRACOS registry that included 407 patients admitted for NSTE-ACS. We were interested to find general characteristics, the time to coronary angiography, mortality and in-hospital complications. A total of 407 patients were included in our study. Nearly half of our patients (49.5%) were considered at high cardiovascular risk. The average to coronary angiography was 5.09 days. Patients who underwent early coronary angiography were significantly younger (p=0.01), had a lower incidence of diabetes (p=0.01), left heart failure (p=0.0001) and electrical changes suggestive of ischemia (p=0.009). Patients who have undergone an invasive strategy had significantly lower levels of creatinine (p<0.0001) and significantly lower GRACE score (p=0.0001). The absence of renal failure, the absence of left ventricular failure, a low GRACE score and the absence of anemia were independent predictors of use of an invasive strategy. The overall mortality among patients included in the study was 2.9%. High heart rate (p=0.04), presence of heart failure (p=0.01), a high serum creatinine (p<0.001) and GRACE score (p<0.0001) were predictors of mortality in ACS ST (-) in our population. The group that underwent early coronary angiography had a statistically significant reduction in MACE (3.4% vs. 15.7%, p=0.04). Despite the fact that our work has showed that invasive strategy is associated with a better prognosis in ACS ST (-) patients, the use of this strategy remains insufficient.

Acute Lung Injury Is an Independent Risk Factor for Brain Hypoxia After Severe Traumatic Brain Injury

Pulmonary complications are frequently observed after severe traumatic brain injury (TBI), but little is known about the consequences of lung injury on brain tissue oxygenation and metabolism. We examined the association between lung function and brain tissue oxygen tension (PbtO2) in patients with severe TBI. We analyzed data from 78 patients with severe, nonpenetrating TBI who underwent continuous PbtO2 and intracranial pressure monitoring. Acute lung injury was defined by the presence of pulmonary infiltrates with a PaO2/FiO2 (PF) ratio less than 300 and the absence of left ventricular failure. A total of 587 simultaneous measurements of PbtO2 and PF ratio were examined using longitudinal data analysis. PbtO2 correlated strongly with PaO2 and PF ratio (P < .05) independent of PaCO2, brain temperature, cerebral perfusion pressure, and hemoglobin. Acute lung injury was associated with lower PbtO2 (34.6 +/- 13.8 mm Hg at PF ratio >300 vs 30.2 +/- 10.8 mm Hg [PF ratio 200-300], 28.9 +/- 9.8 mm Hg [PF ratio 100-199], and 21.1 +/- 7.4 mm Hg [PF ratio <100], all P values <.01). After adjusting for intracranial pressure, Marshall computed tomography score, and APACHE II (Acute Physiology and Chronic Health Evaluation) score, acute lung injury was an independent risk factor for compromised PbtO2 (PbtO2 <20 mm Hg; adjusted odds ratio: 2.13, 95% confidence interval: 1.21-3.77; P < .01). After severe TBI, PbtO2 correlates with PF ratio. Acute lung injury is associated with an increased risk of compromised PbtO2, independent from intracerebral and systemic injuries. Our findings support the use of lung-protective strategies to prevent brain hypoxia in TBI patients.

Pathophysiology of Acute Lung Injury

The acute respiratory distress syndrome (ARDS) is a life-threatening syndrome that may occur in any patient without any predisposition and that is mostly triggered by underlying processes such as sepsis, pneumonia, trauma, multiple transfusions, and pancreatitis. ARDS is defined by (1) acute onset, (2) bilateral infiltrates in chest x-rays, (3) absence of left ventricular failure, and (4) severe arterial hypoxemia with a PaO2/FiO2 ratio less than 200 mmHg. Still, ARDS is feared (mortality 30-40%) and relatively frequent (incidence between 13.5 per 100,000 to 75 per 100,000). Acute lung injury (ALI) describes a similar, but less severe, clinical condition, with PaO2/FiO2 values between 200 and 300 mmHg. Despite ongoing and intensive scientific research in this area, the mechanisms underlying ALI/ARDS are still not completely understood, and until recently, there were no studies demonstrating any beneficial effect of a single treatment modality in ARDS. The recent report that a specific approach to ventilatory support can significantly reduce mortality in ARDS underscores the need for better understanding of the pathophysiological events occurring in this syndrome. This review therefore summarizes the current pathophysiological concepts underlying the evolution of acute hypoxemic respiratory failure and focuses on: (1) possible reasons for the development of ALI/ARDS; (2) cellular and humoral mediator responses leading to a sustained and self-perpetuating inflammation of the lung; (3) consequences with regard to fluid balance, pulmonary perfusion, ventilation, and efficiency of gas exchange; and (4) mechanisms underlying the aggravating complications commonly seen in ARDS, especially ventilator-associated lung injury, ventilator-associated pneumonia, and lung fibrosis.

Threshold values of colloid-osmotic pressure, serum albumin or protein during perioperative period

The water flux across the capillary membrane is directly related to a gradient of hydrostatic and colloid osmotic forces. The membrane is not an absolute barrier to proteins. Any change in the capillary permeability tends to decrease the plasmatic colloid osmotic pressure. The interstitial space includes a perimicrovascular space and a compliant connective tissue space, where oedema accumulates. The lymphatics may easily drain excess filtration, but cannot clear constituted oedema. Primarily, the risk of pulmonary oedema determines the lower limit of the colloid osmotic pressure. During the perioperative period, any extrapolation of the colloid, osmotic pressure from protidaemia or albuminaemia would be approximate. Two major conclusions can be drawn from the results of Guyton and Lindsey. First, in the absence of left ventricular failure, a 50% decrease in colloid osmotic pressure does not increase extravascular lung water. Second, in the case of left ventricular failure, when the left atrial pressure exceeds 10 mmHg, a 50% decrease in colloid osmotic pressure significantly increases the risk of pulmonary oedema. In these experiments, an impairment in capillary membrane permeability is likely. As a result, the threshold at which extravascular water starts to accumulate cannot be precisely defined. However, in the perioperative period, capillary membrane permeability is frequently altered by the acute phase reaction. Finally, in most perioperative clinical situations, a 50% decrease in colloid osmotic pressure may not require any treatment.

Influence of right bundle branch block on short- and long-term survival after acute anterior myocardial infarction

The impact of right bundle branch block on long-term prognosis after anterior wall myocardial infarction is unclear. In 932 patients with Q wave anterior infarction, the short- and long-term prognostic significance of the presence of right bundle branch block was analyzed. Compared with 754 patients without block, 178 patients with right bundle branch block after myocardial infarction showed an increased incidence of left ventricular failure (72% versus 52%, p < 0.001) and increased in-hospital (32% versus 8%. p < 0.001) and 1 year after hospital discharge (17% versus 7%, p < 0.001) cardiac mortality rates.The presence of right bundle branch block was an independent predictor of increased in-hospital and 1-year mortality when entered in a multivariate analysis. However, the absence of left ventricular failure identified a subgroup of patients with right bundle branch block with low in-hospital (4%) and 1 year postdischarge (5%) cardiac mortality rates comparable with those of patients with neither failure nor right bundle branch block (1.7% and 4.8%, respectively). In the presence of left ventricular failure, patients with associated right bundle branch block had higher in-hospital (43% versus 14%, p < 0.01) and 1 year postdischarge (24% versus 9%, p < 0.01) cardiac mortality rates than those of patients with failure but no right bundle branch block.Thus, the presence of right bundle branch block after anterior myocardial infarction is an independent marker of poor prognosis. However, the increased mortality rate is found only in patients with evidence of left ventricular failure and these patients may benefit from early exercise testing and coronary angiography and consideration of revascularization. Patients without left ventricular failure have a favorable 1 year survival rate comparable with that of patients without right bundle branch block.

The effects of oral isosorbide 5-mononitrate on mortality following acute myocardial infarction: A multicentre study*

We have conducted a randomized, double-blind, placebo-controlled multicentre trial of oral isosorbide 5-mononitrate (ISMN) in 360 patients with suspected acute myocardial infarction. Patients were stratified prior to analysis according to the presence or absence of left ventricular failure on admission. ISMN caused a significant reduction in systolic and diastolic blood pressure during the first 12 h. There was no significant effect on heart rate. Overall mortality was 4.9% in the ISMN group compared with 4.0% in controls at 5 days, and 14.1% compared with 10.5% at 6 months (NS). A non-significant reduction in mortality in the ISMN group with heart failure (ISMN 7.9%, placebo 12.9%, at 5 days) contrasted with a non-significant increase in mortality in patients without heart failure treated with ISMN (ISMN 4.1%, placebo 2.1%, at 5 days). Lignocaine was used in twice as many patients in the ISMN group as in placebo group (P less than 0.01), both with and without heart failure. Diamorphine usage was similar in the ISMN and control groups. Oral ISMN has similar haemodynamic effects to intravenous nitroglycerin, and can be of benefit in acute myocardial infarction with heart failure. However, our results question the use of nitrates in acute myocardial infarction in the absence of heart failure.

Nifedipine Following Acute Myocardial Infarction-Dependence of Response on Baseline Haemodynamic Status

The haemodynamic effects of nifedipine (20 mg sublingually) were studied in 40 patients with acute myocardial infarction within 18 h of the onset of symptoms. To determine the influence of preload and afterload on the haemodynamic response to nifedipine, patients were prospectively stratified equally into four groups of 10 patients based on systemic blood pressure level (less than or greater than 160/100 mm Hg) and level of left ventricular filling pressure [pulmonary artery-occluded pressure (PAOP) less than or greater than 18 mm Hg]. In all groups, nifedipine reduced systemic arterial pressure (p less than 0.01) and vascular resistance index (p less than 0.01); heart rate (p less than 0.01) and cardiac index (p less than 0.01) were increased. PAOP was reduced by nifedipine only in those hypertensive patients in whom it was initially raised; in these patients cardiac stroke volume index also increased (p less than 0.01). In hypertensive patients with normal PAOP the cardiac stroke work index was reduced. In patients with normal systemic and pulmonary arterial pressures, nifedipine had no beneficial effects on cardiac function. These data suggested that haemodynamic criteria may allow selection of patients for nifedipine therapy following myocardial infarction; clear advantages were evident only in hypertensive patients in both the presence and the absence of left ventricular failure.

Comparison of intravenous nitroglycerin and sodium nitroprusside in acute myocardial infarction

Initial studies from our institution demonstrated beneficial antiischemic effects of short-term infusion of intravenous nitroglycerin in patients with acute myocardial infarction. At lower doses, nitroglycerin was shown to be principally a venodilator; at higher doses, a mixed venous and arterial dilating effect was demonstrated. The acute hemodynamic effects of nitroglycerin varied in the presence or absence of left ventricular failure; patients with the most severe degree of left ventricular dysfunction had the most beneficial hemodynamic effect. Similar differential effects have been demonstrated for nitroprusside in other studies. A comparison of the arterial vasodilating potency of nitroglycerin and nitroprusside in patients in whom acute hypertension develops following coronary artery bypass surgery revealed that equal lowering of arterial pressure and systemic vascular resistance could be demonstrated in 85 percent of the patients with comparable infusion rates. Review of previous clinical and laboratory studies in animals, in which the effects of nitroglycerin and nitroprusside were compared, in most cases revealed opposite effects on intercoronary collateral flow and, thereby, opposite effects on the severity of regional ischemia. Our recently completed randomized placebo-controlled clinical trial employing a 48-hour infusion of nitroglycerin demonstrated a higher incidence of significant improvement in abnormalities noted on scintigraphy when nitroglycerin treatment was initiated within 10 hours of the onset of symptoms. Beneficial effects of early nitroglycerin treatment have also been demonstrated in previous clinical trials. In similar studies, which utilized nitroprusside infusions in patients with acute myocardial infarction, some investigators found an increase in short-term mortality with early nitroprusside treatment whereas others found benefit. The uniformly favorable results of the clinical trials that utilized intravenous nitroglycerin, although not necessarily supporting its routine use in all patients, would support a preference for nitroglycerin over nitroprusside for the treatment of congestive heart failure and/or acute hypertension complicating acute myocardial infarction.

Cardiopulmonary Effects of Intravenous Fluid Overload: Radiologic Manifestations

Large volumes of normal saline were infused intravenously in 6 dogs until obvious pulmonary edema was observed radiographically. Following volume overload, statistically significant increases occurred in the size of the heart, left atrium, pulmonary arteries and veins, and systemic veins, without the development of congestive heart failure (CHF). The left ventricular end-diastolic pressure remained normal, and cardiac output and stroke volume increased. The results suggest that, in the absence of left ventricular failure, acute volume overload may simulate the radiographic changes produced by CHF. Pulmonary edema may have occurred at least partly from a marked decrease in serum colloid osmotic pressure.

Effects of intravenous nitroglycerin on left ventricular function and ST segment changes in acute myocardial infarction.

It has been shown previously that 30-minute infusions of intravenous nitroglycerin in patients with acute myocardial infarction are able to lower left ventricular filling pressure and improve left ventricular function while lowering mean arterial pressure by only 7 mmHg (0.9 kPa). A decrease in sigmaST in praecordial ST segment mapping studies during nitroglycerin infusion in patients with anterior infarction suggested a decrease in the extent of myocardial ischaemia. In the present study, 30 patients with acute myocardial infarction received 1- to 3-hour infusions of intravenous nitroglycerin at infusion rates sufficient to lower mean arterial pressure by an average of 22 mmHg (2.9 kPa). An improvement in ventricular function was noted in that subgroup of patients with the msot severe left ventricular dysfunction. All patients with anterior myocardial infarction underwent serial ST segment mapping and, irrespective of the presence or absence of left ventricular failure, showed a decrease in sigmaST during nitroglycerin infusion (P less than 0.005). These findings suggest that infusion of nitroglycerin improves left ventricular function and/or alters left ventricular compliance in patients with left ventricular failure complicating myocardial infarction and furthermore decreases sigmaST in all patients, irrespective of the presence or absence of left ventricular failure, suggesting that the extent of myocardial ischaemia is decreased.

Echocardiographic assessment of left ventricular function in aortic valve disease.

Echocardiography was used to study left ventricular size and contraction in 128 patients with isolated aortic valve disease -45 patients with aortic stenosis, 25 with mixed aortic valve disease and 58 with aortic regurgitation. Left ventricular measurements included the end-diastolic internal dimension (LVIDd), mural thickness (PWTd), an index of circumferential myocardial contraction-fractional shortening (FS=[(LVIDd-LVIDs)/LVIDd] X 100)--and stroke volume (LVSV). In the absence of left ventricular failure, measurements in aortic stenosis were characteristic of pressure overload with normal LVIDd and FS and an increase in PWTd related to the severity of stenosis; in aortic regurgitation, there was volume overload with increases in LVIDd and PWTd which were related to the severity of regurgitation, while FS was slightly reduced. In mixed aortic valve disease there was evidence of both pressure and volume overload. When left ventricular failure was associated with aortic stenosis, mixed aortic valve disease and chronic aortic regurgitation, FS was usually reduced. By contrast, in a recent patient with acute severe aortic regurgitation, FS was normal despite left ventricular failure, suggesting pump rather than myocardial failure.

Prosthetic aortic valvular endocarditis.

Infective endocarditis (IE) continues to be one of the most serious complications following cardiovascular surgery, particularly that for replacement of valves. In order to define more clearly the clinical course and the role of surgical therapy, clinical and necropsy data were reviewed in 16 adult patients with prosthetic aortic valvular endocarditis (PAVE) and compared with the experience cited in the literature. Positive blood cultures were obtained in each of the patients with bacterial endocarditis. Gram positive bacteria predominate and the onset of infection is usually later than 25 days postoperatively. In 11 of 16 patients, aortic insufficiency was recognized. Autopsy material demonstrated large perivalvular abscesses which loosened the attachment of the prosthetic valve in each case and which made successful operation unlikely. Aortic insufficiency appears to be of prognostic importance, since patients who developed aortic insufficiency early in the course of PAVE died. Survivors included patients who made an excellent response to medical therapy and who either did not develop aortic insufficiency or developed aortic insufficiency either late in the course or even after cure of PAVE, Poor response to medical therapy and progressive aortic insufficiency even in the absence of left ventricular failure appear to be indications for prompt surgical replacement of the prosthetic aortic valve.

Acute pulmonary edema in the absence of left ventricular failure.

Two patients have been observed to develop acute repetitive pulmonary edema in the absence of left ventricular failure as evidenced by a normal or near normal left atrial pressure recorded during these periods. Continuous monitoring of the left atrial pressure was made possible by a catheter inserted during open-heart surgery. Both patients suffered brain damage, presumably secondary to cerebral air embolism, and eventually succumbed. Although the authors think that a causal relationship between cerebral damage and pulmonary edema best explains the mechanism in these two patients, this must remain conjectural. Neurogenic pulmonary edema, however, has been assumed to be secondary to elevated left atrial and left ventricular end-diastolic pressures. If a specific relation exists in these patients, the findings herein described strongly suggest that this may not be the mechanism.