Moderate Left Ventricular Failure Research Articles

Left Atrial Myxoma with Mild Left Ventricular Dysfunction— A Case Report

Atrial Myxoma is the most common primary cardiac tumors accounting for about 50% of benign primary cardiac tumors, with the majority located in the left atrium. This is a case of large left atrial (LA) myxoma presented with features of mitral stenosis associated with moderate left ventricular failure (LVF) and mild pulmonary artery hypertension (PAH) The patient improved markedly after tumor excision.Pulse Vol.10 January-December 2017 p.29-33

Abstract 622: Cd44 Plays an Important Role in Regulating Heart Failure Induced Lung Vascular Remodeling and Who Type-2 Pulmonary Hypertension

End-stage left ventricular failure or chronic heart failure (CHF) causes severe lung inflammation, vascular remodeling, WHO type-2 pulmonary hypertension, and right ventricular hypertrophy. However, the molecular mechanism of CHF-induced lung inflammation and remodeling is largely unknown. CD44 is a member of the hyaluronate receptor family of cell adhesion molecules, which has been shown to play a selective role in controlling macrophage and lymphocyte migration. Here we demonstrated that end-stage CHF causes a dramatic increase of CD44 expression in heart and lung in human and mice. Histological staining shows that CD44 is predominantly expressed in leukocytes such as macrophages. Flow cytometry analysis further demonstrates that CD44 is predominantly expressed in F4/80 positive macrophages, CD4+, and CD8+ T cells. CD44 expression is dramatically increased in activated T cell subsets. To further determine the physiological role of CD44 in CHF-induced lung remodeling and type-2 pulmonary hypertension, we studied the effect of CD44 blockade on type-2 pulmonary hypertension development in a group of mice with existing moderate left ventricular failure without apparent lung remodeling. Interestingly, we found that blockade CD44 with blocking antibodies (Abs) significantly attenuate the development of lung vascular and interstitial leukocyte infiltration, lung vascular remodeling, fibrosis, and increase of right ventricular hypertrophy. Blockade CD44 signaling also significantly attenuated further decline of left ventricular ejection fraction in mice with existing LV failure. In addition, we demonstrated that induction of T regulatory cells with IL-2 and IL-2 Abs complex significantly attenuated the infiltration of CD44 positive leukocytes in lung tissue, lung vascular remodeling, lung fibrosis, and right ventricular hypertrophy in mice with existing moderate left ventricular failure. Together, these data indicate an important role of CD44 in left ventricular failure-induced lung inflammation, and type-2 pulmonary hypertension, suggesting that inhibition of CD44 may attenuate heart failure progression and type-2 pulmonary hypertension.

PTU-055 The association of co-existent non-ischaemic cardiac disease with morbidity and mortality following liver transplantation

IntroductionThe risk stratification of potential liver transplant candidates with co-existent non-ischaemic cardiac disease (CD) is particularly challenging given the masking effect of the haemodynamic dysfunction of advanced portal hypertension. Whether...

Ovine Models for Chronic Heart Failure

Testing and optimizing of surgical therapies for chronic heart failure (CHF) requires large animal models. CHF has been induced in several large animal species. Sheep have modest body mass increase and demonstrate docile behavior and are therefore a preferred species in research on surgical therapies for CHF METHODS: A literature search for existing ovine CHF models was performed, using search terms "sheep" and "heart failure". Relevant secondary references were traced. Rapid ventricular pacing produces rapid-onset CHFE Its severity ranges from moderate left ventricular failure to severe biventricular failure, depending on length and frequency of pacing. Its counterpart in human CHF is tachycardia-induced HF since it is reversible upon cessation of pacing. Myocardial damage models include CHF induced by cardiototoxic drugs and ischemia. Ischemia-based models include coronary microembolization, occlusion and ischemia/reperfusion models. The microembolization model is relevant to diabetic cardiomyopathy. Coronary occlusion models exhibit variable functional impairment, some with aneurysm formation, and some with mitral valve regurgitation, depending on occlusion localization. They are relevant to CHF following non-reperfused myocardial infarction. Coronary occlusion/reperfusion models are relevant to the occurrence of human ãã despite coronary artery recanalization. Pressure overload of left and right ventricle is induced by aortic and pulmonary artery banding, respectively. Hypertrophy precedes CHF as in patients with valve stenosis and hypertension. Volume overload is induced by valve damage or shunt creation. Atrioventricular valve regurgitation is the most important clinical counterpart. Several ovine CHF models exist. Since they exhibit important cardiac pathology differences, the choice of model should be based on the specific experimental question.

Spontaneous rupture of a benign cavernous haemangioma of the spleen following thrombolysis

Eur J Vasc Endovasc Surg 25, 476-477 (2003)

Diaphragmatic function in patients with chronic left ventricular failure

The aim of this paper is to evaluate the function of respiratory muscles in-patients with chronic moderate left ventricular failure (LVF), and its contribution to the pathophysiology of dyspnea and fatigue. We have studied 20 male patients with LVF, classes II and III of New York Heart Association (NYHA), mean age 66.9±10 years (GI) and 19 male aged-matched controls without cardiopulmonary disease mean age 64.6±8.4 years (GII). The evaluation included (a) methods derived from volitional manoeuvres, maximal inspiratory pressures at Functional Residual Capacity; maximal expiratory pressures at total lung capacity (TLC); nasal sniff; oesophageal sniff and transdiaphragmatic pressures; (b) methods derived from non-volitional manoeuvres, using bilateral cervical magnetic stimulation of the phrenic nerves, measuring the following twitch pressures (oesophageal, gastric and the transdiaphragmatic). With volitional manoeuvres we have not found statistically significant differences between the two groups: maximal expiratory pressures (cmH 2O), GI 138±42; GII 152±40; P=NS and maximal inspiratory pressures (cmH 2O), GI 74.1±22; GII 85±16; P=NS. However, these values were significantly lower than those obtained with sniff manoeuvres, nasal sniff (cmH 2O), GI 95.6±22; GII 99.6±16; P=NS and oesophageal sniff (cmH 2O), GI 96.2±20; GII 97.5±18; P=NS. There were no significant differences between nasal sniff and oesophageal sniff. Using cervical magnetic stimulation, we also didn't find a significant difference for transdiaphragmatic twitch between groups, but the contribution of the diaphragm to the transdiaphragmatic pressure was lower in patients with LVF since the oesophageal twitch was lower (cmH 2O), GI 11.4±3.4; GII 16.3±6.8; P<0,004. In conclusion, the contribution of the diaphragm to total ventilation in-patients with moderate LVF is preserved. However, its capacity to generate negative intra-thoracic pressures is decreased since there is a significant decrease in oesophageal twitch. So, it seems that the diaphragm is the first inspiratory muscle to be affected in patients with moderate LVF.

The acute haemodynamic effects of nicardipine in patients with chronic left ventricular failure.

Nicardipine is a new slow channel calcium blocker. It has been shown to be effective in the treatment of hypertension and angina pectoris. Nine patients with mild to moderate left ventricular failure were given intravenous infusions of nicardipine and the haemodynamic effects measured. In patients receiving 20 mg of nicardipine, mean cardiac index rose to a peak 1.81 X min-1 X m-2 (64%) above the preinfusion level, stroke volume index rose by 12 ml X m-2 (35%) and heart rate rose by 16 beats X min-1 (20%). There was a significant fall in systemic vascular resistance of 50% manifested by a reduction of 22 mm Hg in systolic blood pressure (18%) and 18 mm Hg in diastolic blood pressure (22%). Pulmonary vascular resistance fell by 45%. Mean pulmonary artery pressure and capillary wedge pressure did not change significantly. This study suggests that concomitant mild to moderate left ventricular failure is not a contra-indication to nicardipine therapy in patients with angina.

Hemodynamic effects of digoxin in acute myocardial infarction in man: A randomized controlled trial

Hemodynamic effects of digoxin in acute myocardial infarction (AMI) have been acknowledged to depend on the basal cardiocirculatory state. In the present study, the effects of digoxin in patients with AMI were evaluated in four hemodynamic subsets, based on the relationship between mean pulmonary capillary wedge pressure (PCWP, in mm Hg) and left ventricular stroke work index (LVSWI, in g-m/m 2): subset 1: normal (≤15 mm Hg) PCWP and normal (≥35 g-m/m 2) LVSWI; subset 2: elevated (>15 mm Hg) PCWP and normal LVSWI; subset 3: reduced (<35 g-m/m 2) LVSWI and normal PCWP; and subset 4: elevated PCWP and LVSWI moderately reduced to a range between 16 and 34 g-m/m 2. Forty patients were admitted to the study and were randomly assigned to one of two groups in each subset: control group (19 patients) and treated group (21 patients). Five patients were randomized into each of the subsets 2, 3, and 4 in both the control and treated groups, while in subset 1 there were four control and six digoxin-treated patients. Control patients were administered a placebo saline solution and digoxin-treated patients received 0.50 mg of the drug intravenously in 20 minutes. The effects of the placebo and of the drug were evaluated at 30, 60, and 90 minutes from the end of the infusion. Hemodynamic data did not vary in the control group, and digoxin did not exert any relevant effect in subsets 1 and 2. After drug infusion, cardiac index (Cl, in L/min/m 2) significantly increased in subset 3 patients. Digoxin markedly improved Cl and reduced mean right atrial pressure and PCWP, along with reduction of triple index and of ECG findings of ischemia in subset 4. It was concluded that digoxin can exert favorable hemodynamic effects during AMI only in patients with moderate left ventricular failure; furthermore, the improved cardiocirculatory state after digitalis in these patients might be associated with a net decrease in myocardial oxygen requirements in spite of enhanced contractility, as a consequence of reduced left ventricular volume and wall tension. The absence of hemodynamic response to digitalis which had been observed in previous studies might have been the consequence of erroneous classification of patients.

Effect of Labetalol on Preload in Acute Myocardial Infarction with Systemic Hypertension

We assessed the effects of labetalol on pulmonary wedge pressure (PWP) and other hemodynamic variables in 18 patients with acute myocardial infarction (AMI) and systemic hypertension (systolic blood pressure greater than 150 mm Hg). According to the initial value of PWP, the patients were separated into two groups of nine patients each: Group 1 (PWP greater than or equal to 15 mm Hg) and Group 2 (PWP less than or equal to 12 mm Hg). Labetalol was infused at increasing rates to lower systolic blood pressure below 130 mm Hg; this optimal rate (mean rates for Groups 1 and 2: 1.8 and 2.1 mg/min, respectively) was maintained for 1 h. Hemodynamic variables were measured before and after 1 h of infusion. Labetalol normalized blood pressure in both groups by a significant decrease in total systemic resistance [22% (p less than 0.001) and 13% (p less than 0.02)] and in cardiac index [17% (p less than 0.005) and 12% (p less than 0.02)]. While the hemodynamic responses were rather similar in both groups, the PWP decreased significantly (from 22 to 15 mm Hg, p less than 0.01) in Group 1, but did not change significantly in Group 2 (from 7 to 10 mm Hg, NS). The possible mechanisms behind these different responses are discussed. We conclude that labetalol is an effective drug for treating systemic hypertension in AMI which acutely decreases total systemic resistance and preload in patients with moderate left ventricular failure.

Hemodynamic effects of digoxin in acute myocardial infarction.

Hemodynamic effects of 0.50 mg of i.v. Digoxin were studied in 25 patients (18 males and seven females, with a mean age of 66.0 ± 8.7 years) with an acute myocardial infarction (AMI) who underwent a right heart catheterization and hemodynamic monitoring in the CCU. Heart rate (HR) was reduced from 97.16 ± 16.41 to 91.00 ± 16.85 beals/min (P < 0.01); cardiac index (CI) increased from a mean value of 2.16 ± 0.49 to 2.55 ± 0.70 l/min/m2 (P < 0.001); stroke index (SI) and left ventricular stroke work index (SWI) also improved from 22.46 ± 4.11 to 28.44 ± 7.61 ml/m2 and from 27.52 ± 5.71 to 36.04 ± 9.65 gm-m/m2 (P < 0001). Systolic (SAP) and diastolic (DAP) arterial pressure slightly but significantly increased (P < 0.01) from 121.56 ±16.61 and 75.08 ± 9.03 mm Hg respectively, to 126.80 ± 16.28 and 77.72 ± 9.25 mm Hg; pulmonary artery mean pressure (PMP) decreased from 22.30 ± 8.22 to 20.48 ± 5.47 mm Hg (P < 0.05). The patients were subdivided into two hemodynamic classes, according to the values of the PMP measured in basal conditions: group 1 (PMP ≤ 19 mm Hg): 11 patients (44.0%); group 2 (PMP > 19 mm Hg): 14 patients (56.0%). Hemodynamic effects of i.v. Digoxin were analysed separately in each class, and the results were compared. No difference was observed between the data from the two groups, except for PMP. This parameter was unchanged after Digoxin in group 1, while in group 2 it was reduced from 26.39 ± 5.29 to 23.18 ± 5.76 mm Hg. Furthermore, HR did not vary and DAP significantly increased only in group 1 (hypovolemic patients) while HR significantly decreased and DAP remained unchanged in the group of patients with a PMP > 19 mm Hg. We concluded that Digoxin treatment during AMI can favourably affect the circulatory conditions primarily in cases with a moderate left ventricular failure. The beneficial effects of the drug seemed to be less evident when administered to patients with almost normal pump function or with extreme degrees of left ventricular failure.

Failure of Methylprednisolone to Protect Acutely Ischemic Myocardium: A Contrast with Subsequent Beta-Adrenergic Blockade in Man

Two grams of methylprednisolone was administratered to ten patients with acute myocardial infarction at an average of 13 hours from the onset of symptoms; pain in the chest was not relieved in six of the ten patients. In one hour, no significant improvement was noted in the function of the ischemic segments (examined using a multiaxis echocardiographic method) or in the S-T segments of the 12-lead electrocardiogram. Left ventricular filling pressure soon increased by an average of 4 mm Hg (P less than 0.005), without ventricular dilatation or a Frank-Starling response, suggesting a decrease (ischemic?) in myocardial compliance. Cardiac output by Swan-Ganz thermodilution later increased by 21 percent (P less than 0.01) when a decrease in peripheral vasoconstriction was evident. In contrast, small-dose beta-adrenergic blockade using 0.2 mg of pindolol intravenously after administration of methylprednisolone immediately relieved pain in the chest in all six patients. Elevation of the S-T segments was reduced by 34 percent (P less than 0.05) within 15 minutes, and the contractile function of the ischemic segments improved markedly, by 3 mm or to 34 percent of normal, from the 4 percent of normal before administration of pindolol (P less than 0.005). Hemodynamic function did not deteriorate in the eight patients with uncomplicated infarction or moderate left ventricular failure. Therapy with pindolol thus reduced clinical, electrocardiographic, and myocardial mechanical signs of acute ischemia safely, while administration of methylprednisolone had no short-term protective effect.

Serial measurements of left ventricular ejection fraction by radionuclide angiography early and late after myocardial infarction

The left ventricular ejection fraction was determined serially with radioisotope angiography in 63 patients with acute myocardial infarction. After the peripheral injection of a bolus of technetium-99m, precordial radioactivity was recorded with a gamma scintillation camera and the ejection fraction calculated from the high frequency left ventricular time-activity curve. Since this technique requires no assumptions with respect to left ventricular geometry, it is particularly useful in patients with segmental left ventricular dysfunction. Serial measurements during the first 5 days after hospital admission were made in 50 patients, 30 of whom were studied during the subsequent 2 to 39 months (mean 19.9 months). Late follow-up serial studies were also performed in an additional 13 patients who had only one measurement of the left ventricular ejection fraction during the early postinfarction period. Early after infarction, the left ventricular ejection fraction was normal (more than 0.52) in only 15 of the 63 patients, and averaged 0.52 ± 0.05 (standard deviation) in the 27 patients with an uncomplicated infarct. The ejection fraction was reduced in 24 patients with mild to moderate left ventricular failure (0.40 ± 0.05, P < 0.0001) and in the 12 patients with overt pulmonary edema (0.33 ± 0.07, P < 0.0001). In 35 patients the ejection fraction correlated with the mean pulmonary arterial wedge pressure ( r = 0.72). In 15 patients with normal left ventricular wall motion by heart motion videotracking, the ejection fraction was significantly higher (0.53 ± 0.08) than in the 26 patients with regional left ventricular dysfunction (0.41 ± 0.10, P < 0.0001). During the early postinfarction period, the left ventricular ejection fraction improved in 55 percent of patients and remained unchanged or decreased in 45 percent. A further increase in the ejection fraction was noted in 61 percent of patients during the late follow-up period. Patients with an initially low or decreasing ejection fraction had a significantly greater incidence of early mortality and left ventricular dysfunction ( P < 0.02) than those whose ejection fraction was normal or improved to normal early after infarction. These data indicate that the ejection fraction is a sensitive indicator of left ventricular function after acute myocardial infarction and that serial measurements are helpful in predicting early mortality and morbidity.

Echoventriculography in acute myocardial infarction. III: Clinical correlations and implication of the noninfarcted myocardium

Echoventriculography permits detection of regional abnormalities of left ventricular wall motion in acute myocardial infarction. Overall and regional performance of the left ventricle was related to the prognosis and clinical severity of acute transmural myocardial infarction in 30 patients. Although values for left ventricular size, ejection fraction and modified mean circumferential fiber shortening velocity were all abnormal ( P < 0.005), they did not differ among 8 patients with uncomplicated infarction, 12 with moderate left ventricular failure and 10 with pulmonary edema or shock. In contrast, magnitude of the summed wall motion amplitudes from seven standard regions around the left ventricle decreased in parallel with ejection fraction ( P < 0.001) and with clinical severity of infarction ( r = −0.79, P < 0.001). Function of the healthy myocardium was hypercontractile in 40 percent of patients, but this occurred only in patients with uncomplicated or moderately severe infarction. In patients with severe pump failure the “uninvolved” myocardium did not manifest a hypercontractile or even normal response despite infusion of catecholamines (−21 percent; r = −0.76, P < 0.001). Four nonsurviving patients had the poorest ventricular function (as low as 10 percent of normal) as assessed by several segmental echocardiographic performance indexes. Performance of the noninfarcted myocardium therefore seems to have a role in deterioration of left ventricular pump function in acute myocardial infarction.

Use of sublingual nitroglycerin in congestive failure following acute myocardial infarction.

The effect of 0.3 mg sublingual nitroglycerin (NTG) was evaluated by hemodynamic measurements and precordial S-T-segment mapping in 17 patients following acute myocardial infarction. In all cases NTG produced a prompt reduction in mean pulmonary capillary wedge pressure (PCW) from an average of 19 ± 2 to 14 ± 1 mm Hg associated with a small fall in mean arterial pressure from a mean of 85 ± 4 to 82 ± 4 mm Hg. No significant change in heart rate occurred. In patients without left ventricular failure (PCW 3-12 mm Hg) cardiac output (CO) fell 9%. By contrast, in patients with moderate left ventricular failure (PCW 13-22 mm Hg) CO rose 18%. In three patients with refractory left ventricular failure (PCW 25-31 mm Hg) CO rose 25%. Two of these patients were treated with repetitive NTG doses in addition to previously ineffective diuretic therapy with resolution of resistant pulmonary edema. No significant changes in the magnitude of S-T-segment elevations were noted. NTG may have a special role in the management of acutely ill patients with myocardial infarction in whom pulmonary edema does not respond to conventional therapy.