Left Heart Dysfunction Research Articles

Clinical Relevance of Echocardiography in Acute Severe Dyspnea

The aim of this study was to assess the most relevant echocardiographic parameter for the clinical diagnosis of acute dyspnea due to left-heart dysfunction. Transthoracic echocardiography was performed in 88 patients in sinus rhythm admitted for respiratory distress. Two experts determined the cause of dyspnea as cardiogenic (26 patients) or noncardiogenic (62 patients). The feasibility was 100% for the E/A ratio and the E/E deceleration time (EDT) ratio but 97%, 89%, and 85% for the E/Ea ratio, left ventricular ejection fraction (LVEF), and the E/propagation velocity (Vp) ratio, respectively. The area under the receiver operating characteristic curve for E/EDT (0.947 +/- 0.035) was statistically significantly greater than that for E/A (0.753 +/- 0.068) (P = .004). The areas under the curves for all other parameters were not statistically significantly different. In the subpopulation of patients with LVEFs > 45%, the area under the curve for LVEF was significantly smaller than those for E/Ea, E/EDT, and E/Vp. E/EDT, E/Ea, and E/Vp appear equally useful to distinguish acute dyspnea due to left-heart dysfunction from that of pulmonary origin. However, E/EDT and E/Ea can be considered the best indices with regard to feasibility.

Invited Commentary

This retrospective study by Khandhar and colleagues [1Khandhar S. Varadarajan P. Turk R. et al.Survival benefit of aortic valve replacement in patients with severe aortic regurgitation and pulmonary hypertension.Ann Thorac Surg. 2009; 88: 752-757Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar] evaluates the effect of aortic valve replacement (AVR) for severe aortic regurgitation (AR) in the setting of pulmonary hypertension (PHT). In this cohort of patients, AVR is safe and translates into a survival benefit at 5 years. Although the study is small, it offers a timely opportunity to reconsider indications for AVR and the underlying pathophysiology of left-heart causes of PHT. Current American College of Cardiology/American Heart Association recommendations for AVR do not include PHT. We know that untreated AR results in left ventricular dilation, dysfunction, and eventually, PHT [2Basu B. Cherian G. Krishnaswami S. Sukumar I.P. John S. Severe pulmonary hypertension in advanced aortic valve disease.Br Heart J. 1978; 40: 1310-1313Crossref PubMed Scopus (15) Google Scholar]. Severe AR also results in endothelial injury within the pulmonary vasculature, interstitial edema, and fibrosis, all of which contribute to increased pulmonary artery vascular tone. Furthermore, severe right ventricular dysfunction can result in chronic small emboli to the lungs and worsen the disease process, and likely blunt postoperative recovery. Indeed, these pulmonary insults are the consequences of prolonged disease. The reality of prolonged disease before surgical intervention raises two questions: whether PHT should be an indication for AVR and whether we are waiting too long to perform AVR in this population. At present, there is a class IIa recommendation to perform AVR in asymptomatic patients with evidence of severe left ventricular dysfunction, defined as end-diastolic dimension exceeding 75 mm or end-systolic dimension exceeding 55 mm. For women, in particular, this degree of left-heart dysfunction may be too severe to expect AVR to improve the clinical outcome. Further clarification of the effect of mitral valve function will also be helpful. Mitral stenosis and regurgitation both result in increased pulmonary vascular resistance and contribute to elevated pulmonary artery pressures. The mitral effective regurgitant orifice and mitral deceleration time have been shown to strongly correlate with elevated pulmonary artery pressures [3Enriquez-Sarano M. Rossi A. Seward J.B. Bailey K.R. Tajik A.J. Determinants of pulmonary hypertension in left ventricular dysfunction.J Am Coll Cardiol. 1997; 29: 153-159Abstract Full Text Full Text PDF PubMed Scopus (232) Google Scholar]. Khandhar and associates [1Khandhar S. Varadarajan P. Turk R. et al.Survival benefit of aortic valve replacement in patients with severe aortic regurgitation and pulmonary hypertension.Ann Thorac Surg. 2009; 88: 752-757Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar] appropriately call our attention to mitral valve function in this cohort: 16 of the 32 patients receiving AVR had mitral valve repair (n = 8) or replacement (n = 8). Definitive aortic and mitral valve procedures may be necessary to restore left-sided hemodynamics and filling pressures. In fact, the lack of mitral regurgitation may suggest secondary causes of PHT at work. As we reconsider our indications for AVR in the setting of PHT, new screening variables and closer attention to mitral valve function will be essential. Survival Benefit of Aortic Valve Replacement in Patients With Severe Aortic Regurgitation and Pulmonary HypertensionThe Annals of Thoracic SurgeryVol. 88Issue 3PreviewSevere pulmonary hypertension occurs in approximately 10% of patients with severe aortic regurgitation (AR). The potential survival benefit of aortic valve replacement (AVR) in these patients is not known, and was analyzed in a large cohort of patients. Full-Text PDF

Cardiac Dysfunction After Left Permanent Cerebral Focal Ischemia

Stroke can lead to cerebrogenic cardiac arrhythmias. We sought to investigate the effect of ischemic stroke on cardiac function in a mouse model of permanent middle cerebral artery occlusion (pMCAO). Twenty-four hours after the induction of focal ischemia, cardiac function was measured in mice by endovascular catheterization of the heart. Immediately after hemodynamic measurements, mice were euthanized and brains were excised and sectioned to measure infarct volume and the severity of insular cortex injury. Myocardial damage was evaluated by hematoxylin-eosin staining. Serum and heart levels of norepinephrine (NE) were also determined. Cardiac dysfunction occurred in 9 out of 14 mice that underwent left pMCAO. In these 9 mice, the severity of left insular cortex lesion was greater than the mice with normal heart function. The serum and heart levels of NE were significantly higher in left pMCAO mice with heart dysfunction. Liner regression analysis indicates significant inverse correlation between the severity of left insular cortex damage and heart dysfunction. Mice that underwent right pMCAO did not exhibit cardiac dysfunction. This study shows that left focal cerebral ischemia can produce cardiac dysfunction, which is associated with the extent of left insular cortex damage. Furthermore, mice exhibiting cardiac dysfunction had elevated levels of NE in the serum and heart.

Detection of acute heart failure in chronic obstructive pulmonary disease patients: role of B-type natriuretic peptide

Unrecognized chronic heart failure is present in 21-30% of chronic obstructive pulmonary disease patients. It may be a precipitating factor for acute exacerbation of chronic obstructive pulmonary disease or may hinder weaning from mechanical ventilation. The aim of the review is to emphasize recent studies that validated measurements of plasma B-type natriuretic peptide in the diagnosis of heart dysfunction in chronic obstructive pulmonary disease patients. Measurements of B-type natriuretic peptide or N-terminal pro-B-type natriuretic peptides are accurate in the diagnosis of left heart dysfunction in chronic obstructive pulmonary disease patients either in stable condition or during acute exacerbation of chronic obstructive pulmonary disease. Natriuretic peptide thresholds are elevated in comparison to cut-offs usually reported in patients without pulmonary disease. B-type natriuretic peptide dosage is also able to uncover new onset of left heart failure associated with weaning difficulties from mechanical ventilation in chronic obstructive pulmonary disease patients. Recent evidence suggests that natriuretic peptide measurements are accurate in the diagnosis of coexisting left heart failure in chronic obstructive pulmonary disease patients, either in stable condition or during severe cardiopulmonary interactions occurring during acute exacerbation of chronic obstructive pulmonary disease, or evoking weaning difficulties related to left heart dysfunction.

Overview of Cardiac Status in Thalassemia Intermedia: The Lebanese Experience.

Introduction: Thalassemia intermedia (TI) is a heterogeneous genetic disease affecting the β-globin chain of the hemoglobin molecule resulting in a unique and wide clinical spectrum. The majority of TI patients are mildly anemic requiring merely occasional blood transfusions. Their mild anemia might be tolerable at a young age but over years it is proven to cause multiple system damage due to the chronic hypoxic and compensatory states. One of the systems affected, and the number one cause of mortality in this group, is the cardiovascular system. In this study we tried to assess echocardiographically the global left heart condition in TI patients and its relation to haematologic measurable variables (NT-proBNP, Ferritin, Hb, and HbF) as well as liver iron concentration (LIC).Subjects and Methods: A total of 74 patients were enrolled in our observational, case-series study having already met the conventional clinical and genetic criteria for diagnosing TI. LIC was measured by R2* MRI for all of the 74 patients who were then referred to an outpatient clinic for cardiac evaluation and echocardiographic testing between December 2006 and June 2007. Blood samples were also collected for measuring NT-proBNP levels in a random subgroup of 19 patients.Results: Of the 74 TI patients, 33 were male and 41 were female with a mean age of 26.54 (range 8–63) years and body surface area (BSA) of 1.54 (range 0.82–2.14) m2. Their mean hemoglobin was 8.43 (range 4.90–13.10) g/dl having a mean serum ferritin of 1023 (range 15–4140) ng/mL, a mean LIC of 9.00 (range 0.5–32.1) mg/g, and a mean NT-proBNP of 113.50 (range 16.42–371). The majority 59 (79.7%) had undergone splenectomy with only 11 (14.86%) maintained on iron chelation. Pulmonary hypertension (PHT) defined as peak systolic tricuspid gradient >30 mm Hg was present in 15 (38.5%) of our TI patients group excluding 35 patients with undetected tricuspid regurgitation. LV dilatation was significantly above the normal range in 48 (68.57%) patients. Left ventricular mass index (LVMI) was increased in 34(49.27%) patients; and all of them showed eccentric hypertrophy. The left ventricular ejection fraction (LVEF) was within normal range for most of the patients; only 3 had LVEF <55%. There was a negative correlation between LVEF and LIC with borderline significance (r = −0.22; p=0.061) but not between LVEF and ferritin (r = 0.06; p=0.61). NT-proBNP was above upper limit of normal in 7(36.8%) patients of the subgroup. It was significantly and negatively correlated with hemoglobin (r = −0.49; p = 0.032) but not with age, LIC, mean serum ferritin, left ventricular end-diastolic diameter, LVMI, LVEF, or Doppler indices.Conclusion: Although TI patients primarily develop PHT leading to right heart failure, our study has shown that many do exhibit sub-clinical left heart dysfunction (characterized by LV dilation and/or eccentric hypertrophy) as well. Knowing that iron overload correlates better with LIC than with ferritin in TI and after showing that LIC is negatively (but weakly) correlated with LVEF, iron overload might be a contributing factor to LV dysfunction similar to that encountered in TM. Finally; NT-proBNP is found to be negatively related only to hemoglobin level which adds to the poor prognosis of the profoundly anemic TI patients.

Infiltration of Inflammatory Cells Plays an Important Role in Matrix Metalloproteinase Expression and Activation in the Heart during Sepsis

Septicemia is an emerging pathological condition involving, among other effects, refractory hypotension and heart dysfunction. Here we have investigated the contribution of resident nonmyocytic cells to heart alterations after lipopolysaccharide administration. These cells contributed to the rapid infiltration of additional inflammatory cells that enhance the onset of heart disease through the release of inflammatory mediators. Early activation of resident monocytic cells played a relevant role on the infiltration process, mainly of major histocompatibility complex class II- and CD11b-positive cells. This infiltration was significantly impaired in animals lacking the nitric-oxide synthase-2 (NOS-2) gene or after pharmacological in-hibition of NOS-2 or cylooxygenase-2, suggesting a significant contribution of nitric oxide and prostanoids to the infiltration process. Under these conditions, the expression of NOS-2 and cylooxygenase-2 in the whole organ was attenuated because cardiomyocytes failed to express these enzymes. However, cardiomyocytes expressed and activated matrix metalloproteinase-9 through mechanisms regulated, at least in part, by nitric oxide and prostaglandins in an additive way. These results directly link the inflammatory response in the heart and extracellular matrix remodeling by the matrix metalloproteinases released by the cardiomyocytes, suggesting that activation and recruitment of inflammatory cells to the heart is a major early event in cardiac dysfunction promoted by septicemia.

Clinical differences between idiopathic and scleroderma‐related pulmonary hypertension

Pulmonary arterial hypertension related to scleroderma (PAH-Scl) is associated with high morbidity and mortality as well as poorer response to therapy and worse outcomes compared with the idiopathic form of PAH (IPAH). Scleroderma is an autoimmune disease that can affect left and right heart function directly through inflammation and fibrosis and indirectly through systemic and pulmonary hypertension. This study tested the hypothesis that an increased prevalence of left heart disease might explain the higher mortality in patients with PAH-Scl compared with patients with IPAH. The study was designed as a retrospective cohort study comparing the baseline clinical data from 91 consecutive patients (41 with IPAH and 50 with PAH-Scl). Cox proportional hazards models were used to predict the effect of clinical covariates on patient survival. Patients with PAH-Scl had a lower mean pulmonary artery pressure (46.6 mm Hg versus 54.4 mm Hg in patients with IPAH; P = 0.002) despite similar levels of cardiac dysfunction (cardiac index 2.2 and 2.1 liters/minute/m(2), respectively; P = 0.19). Echocardiography revealed similar degrees of right ventricular dysfunction in the 2 groups, whereas a predominance of left heart dysfunction was observed in patients with PAH-Scl. One- and three-year survival estimates were 87.8% and 48.9%, respectively, in patients with PAH-Scl and 95.1% and 83.6%, respectively, in those with IPAH. Patients with PAH-Scl were 3.06 times more likely to die than were patients with IPAH, after controlling for the presence of pericardial effusion; there was no significant change in increased risk of death in PAH-Scl after controlling for left heart disease. The results confirm that there are significant clinical and survival differences between IPAH and PAH-Scl. The presence of left heart disease, although more common in PAH-Scl, was not predictive of the higher mortality in these patients.

The Utility of Impedence Cardiography in Assessment of Hemodynamics in Patients with Left and Right Heart Dysfunction: Fact Versus Fiction

The Utility of Impedence Cardiography in Assessment of Hemodynamics in Patients with Left and Right Heart Dysfunction: Fact Versus Fiction

Association of Left-Heart Dysfunction with Severe Exacerbation of Chronic Obstructive Pulmonary Disease

Cardiac biomarkers are used to distinguish acute dyspnea due to left-heart dysfunction from that of pulmonary origin. However, they have not been assessed in the specific setting of acute exacerbation of chronic obstructive pulmonary disease (AECOPD), where they might be released without left-heart impairment. To assess the accuracy of troponin T and of amino-terminal pro-brain natriuretic peptide (NT-proBNP) in the diagnosis of AECOPD associated with left ventricular (LV) dysfunction. Both biomarkers were measured in 148 consecutive patients on intensive care unit admission for AECOPD. A panel of physicians adjudicated blindly the cause of AECOPD to be unlikely, possibly associated, or definitely associated with LV dysfunction. The final diagnosis was AECOPD definitely associated with acute left-heart dysfunction in 31.1%, possibly associated with LV dysfunction in 13.5%, and probably not associated with LV dysfunction in 55.4%. Both NT-proBNP and troponin T levels were significantly different among the three groups. The area under the receiver operating characteristic curve was greater for NT-proBNP (0.95 vs. 0.67). A cutoff of 1,000 pg/ml was accurate to rule out left-heart involvement in AECOPD (sensitivity, 94%; negative predictive value, 94%; negative likelihood ratio, 0.08). A cutoff of 2,500 pg/ml had the best operating characteristics to rule in the diagnosis (positive likelihood ratio, 5.16). Left-heart involvement in AECOPD was the only variable independently associated with increased secretion of NT-proBNP (odds ratio, 74; 95% confidence interval, 15-375; p = 0.0001). NT-proBNP and troponin T are useful in excluding AECOPD associated with left ventricular dysfunction. NT-proBNP was the more accurate of the two.

Failing older hearts? Of myths and left-overs

The failing heart is the common endpoint of all cardiac disease. While the syndrome of ‘heart failure’ encompasses both left and right heart dysfunction, impairment of left ventricular (LV) function carries the greatest consequences. Failure of contraction, or LV systolic dysfunction, is usually the result of epicardial coronary artery occlusion, with resultant muscle necrosis and myocardial scarring. Failure of myocardial relaxation, loosely termed ‘diastolic’ heart failure, usually results from connective tissue changes. These are typically seen in chronic hypertension and result from mechanical load disturbance but may also be the result of chronic metabolic imbalance – possibly through long-term smallvessel ischaemia.

Tricuspid replacement and short-term follow-up: summary of 42 cases

To summarize the experience in tricuspid valve replacement (TVR). From March 1997 to June 2004, 42 patients underwent isolated or combined TVR. Of the cases, 20 cases had prior cardiac operation (tricuspid valve had been repaired in 8). Indication of TVR: (1) irreparable and/or progressive tricuspid lesions; (2) intolerable tricuspid dysfunction after tricuspid repair. Instead of tricuspid repair, TVR was preferred when one of the following co-existed: moderate to severe increase of pulmonary vascular resistance; residual left heart dysfunction; previously repaired tricuspid. Simultaneous replacement after unsuccessful tricuspid repair had to be done in 14 cases. Valve replacement combinations were isolated TVR in 30 cases, tricuspid and aortic and mitral in 8, tricuspid and mitral in 3, tricuspid and aortic in 1. Fourteen tissue and 28 bi-leaflet mechanical valve prostheses were used in the tricuspid position. Other simultaneous procedures included corrections of congenital anomalies in 10 patients, repair of peri-prosthetic leakage, resection of myxoma and coronary artery bypass grafting in 1 case each. The operative mortality was 17%, and mortality 31%. Four patients died of low cardiac output. Massive cerebral thromboembolism, renal failure and dyscrasia was the cause of death in 1 case each. Post-operative heart function NYHA classification: 21 cases in I, 10 in II, 1 in III and 1 in IV. Late death occurred in 2 cases. TVR is preferable for a severely damaged or deformed tricuspid valve if the possibility of successful repairing is small, especially when accompanied pulmonary vascular disease and uncorrected lesions and/or dysfunction of the left heart co-exists.

An Integrative Cardiovascular Model of the Standing and Reclining Sheep

We have developed an integrative model of the ovine cardiovascular system that simulates the effects of posture and ventricular function to help design the circulatory and pulmonary assist devices often tested in conscious sheep that stand and recline during chronic experiments. Our present focus is the simulation itself and not the evaluation of specific assist devices. Adjusted parameters of the model provide good fits to in vivo experimental data and can describe the hemodynamic changes that follow balloon occlusion of the inferior vena cava and standing. Since circulatory assist devices are often tested in animal preparations of left heart failure, we extended the model to study the effects that standing and inferior vena cava occlusion would have in sheep with primarily systolic left heart dysfunction. We also developed an elastance-based formulation for ventricular muscular work and a sensitivity analysis of the autonomic reflexes affecting blood pressure. The model can analyze the biophysical mechanisms underlying the responses to orthostatic stress and left ventricular dysfunction and should help improve the development and testing of assist devices.

THE PROTOTYPE OF TRANS-VENTRICULAR LVAD WITH ROLLING BEARINGS AND A PURGE SYSTEM: TOWARD DURABILITY AND PERFORMANCE

Purpose: To develop a simple plug-and-play Transventricular/transAortic valve LVAD (TA-LVAD) for acute left heart dysfunction designed to just plug into the cardiac apex via a small left thoracotomy to achieve immediate total left ventricular (LV) support. Methods: The LVAD is composed of a motor and an impeller pump within a custom cannula designed to be placed transapical across the LV chamber, through the aortic valve, into the aortic root. The motor has a motor coil with iron core and a rotor with a 4-pole magnet. The pump has a low impact three turbine impeller with an outflow guide vane. The motor is supported by 8 needle roller bearings in each end of the rotor to reduce friction and is purged by a heparin saline infusion to prevent bearing thrombosis. The pump prototype was tested in saline with the outlet connected to 3/8” tubing for flow and pressure head measurements. The preload of the pump was kept at zero mmHg. The pump was operated at 12500, 15000 and 17500 rpm to determine pressure and flow curves. Results: The pump as fabricated had a length of 11.5 cm and weight of 53 grams. The performance property diagram shows: the prototype can pump 4 l/min at 15000 rpm and 9 l/min at 17500 rpm, against 100 mmHg afterload. Conclusion: Our current prototype with a length of 11.5 cm and diameter of 13 mm achieves total left ventricular support and is designed to be easily inserted transapically.

Excessive exercise ventilation in moderate left heart dysfunction. Influence of postural changes in central haemodynamics and blood gases.

To evaluate the relative importance of pulmonary congestion and peripheral hypoxia as causes for the excessive exercise ventilation in left heart dysfunction, seven patients with excessive ventilation and distinct left heart dysfunction during moderate exercise (LHD), and seven control patients with essentially normal exertional functions (CTR), had ventilation, central haemodynamics, arterial and mixed venous blood gases examined at rest and exercise, 32 W (25-40) in the LHD group and 44 W (33-49) in the CTR group, in lying and sitting positions. Change from lying to sitting exercise, led to fall in pulmonary artery wedge pressure (PAWP) from 31.0 +/- 5.5 to 8.8 +/- 5.0 mmHg in the LHD group, compared with from 13.7 +/- 1.0 to 2.1 +/- 2.4 mm Hg in the controls, while ventilation/O2 intake ratio (V/VO2) and physiological dead space/tidal volume ratio (VD/VT) showed a tendency to rise, from 36.3 +/- 8.8 to 39.2 +/- 7.4, and from 0.35 +/- 0.11 to 0.39 +/- 0.09, respectively, in the LHD group, and from 27.5 +/- 3.1 to 28.7 +/- 5.3, and from 0.19 +/- 0.09 to 0.21 +/- 0.12 in the controls. Mixed venous O2 tension (PvO2) showed a marked decline from 3.60 +/- 0.33 to 3.26 +/- 0.36 kPa in the LHD group, as compared with from 3.94 +/- 0.28 to 3.71 +/- 0.29 kPa in the controls, while the calculated physiologic shunt (Qs/Qt) suggested improved alveolo-arterial gas exchange. The data fit in with recent studies ascribing the excessive exercise ventilation to a combination of signals from hypoxia-induced changes, particularly in the exercising muscles, and augmented ergoreflex and central and peripheral chemoreceptor activity, partly to changes in the integrated control of ventilation and circulation, not to mechanisms related to pulmonary congestion.

Left Ventricular Diastolic Dysfunction in Patients with So‐Called Lone Atrial Fibrillation

Lone atrial fibrillation (AF) is defined by the absence of identifiable causes of AF, but its hemodynamics have not been investigated. Twenty-eight patients with lone AF were compared with 14 control patients referred for Wolff-Parkinson-White ablation. Transthoracic and transesophageal echocardiography were performed to rule out structural heart disease, followed by transseptally performed complete hemodynamic evaluation of the left heart systolic and diastolic function. There was no evidence of diastolic dysfunction according to echocardiographic criteria in AF and control patients. There was no difference in echocardiographic measurements, except for a significantly higher inferosuperior left atrial dimension seen in the four-chamber apical view in AF patients (51+/-10 vs 40+/-6 mm, P = 0.03). Hemodynamic evaluation showed that end-diastolic left ventricular pressure and the nadir of the left atrial Y descent were significantly higher in lone AF patients versus controls: 13+/-5 versus 8+/-3 mmHg (P = 0.001) and 6.7+/-3 versus 4.6+/-2.7 mmHg (P = 0.05). Our results demonstrated the presence of diastolic left heart dysfunction in patients with so-called lone AF.

Effects of isosorbide dinitrate on electrocardiography, hemodynamics, and ventilation in patients with exercise-induced elevation of pulmonary artery wedge pressure.

The mechanisms underlying exertional hyperpnea in patients with coronary artery disease and transient left ventricular dysfunction are still not fully understood. The study was undertaken to investigate whether the ventilatory response to exercise reflects the effects of acute medical treatment of exercise-induced left ventricular dysfunction, and to evaluate mechanisms relevant to excessive exertional ventilation. In 11 male patients, aged 65.2 +/- 6.0 years, all with pulmonary artery wedge pressure (PAWP) > 25 mmHg and ST depression > 2 mm during moderate supine exercise, ventilation (V), oxygen uptake (VO2), hemodynamics, electrocardiogram (ECG), and arterial and mixed venous blood gases were examined during supine rest and exercise, before and at hourly intervals after peroral intake of 30 mg isosorbide dinitrate (ISDN). Six similar patients were examined with the same protocol without ISDN administration and comprised a control group. Before administration of ISDN, exercise PAWP was 35.3 +/- 5.9 mmHg, ECG showed 2.77 +/- 1.06 mm ST depression, and V/VO2 was 31.8 +/- 4.8 l/l. One h after ISDN administration, exercise mean PAWP was 11.0 +/- 2.5 mmHg (p < 0.001), ST depression 0.59 +/- 0.8 mm (p < 0.001), whereas V/VO2 was unchanged, 30.1 +/- 5.3 l/l. Two h later, PAWP remained reduced and there were only minor ST depressions, while V/VO2 remained high. Exercise cardiac index (CI) and mixed venous oxygen tension (PvO2), initially 4.7 +/- 0.67 l/min/m2 and 3.54 +/- 0.35 kPa, respectively, remained at the same low level throughout the study. In the six nontreated patients, there were no significant changes in ST depression, exercise PAWP, or exertional ventilation. Isosorbide dinitrate treatment markedly improved exercise-induced left heart dysfunction, whereas excessive ventilatory response was unaffected, even after 3 h. Thus, measurements of the exercise hyperpnea did not properly reflect effective reduction of myocardial ischemia.

Myocardial Bridging as a Cause of Acute Transient Left Heart Dysfunction

The significance of myocardial bridging is still a matter of debate, and although several reports have underlined its pathologic potential, myocardial bridging is often considered to be a benign phenomenon. We present here the case of a 63-year-old woman with a history of acute left heart failure and ECG evidence of ischemia, and whose primary abnormality on extensive workup was myocardial bridging. This case further underlines that myocardial bridging can lead to significant cardiac events.

Pediatric lung transplantation

From July 1990 to April 1993, 36 lung transplantations in 33 patients were performed in our pediatric transplant program (0.25 to 23 years, mean age 10.3 years). Eight children had been continuously supported with a ventilator for 3 days to 4.5 years before transplantation and three were supported by extracorporeal membrane oxygenation. Indications for lung transplantation in this pediatric population included the following: cystic fibrosis (n = 13), pulmonary hypertension, and associated congenital heart disease (n = 10), pulmonary atresia, ventricular septal defect and nonconfluent pulmonary arteries (n = 3), pulmonary fibrosis (n = 6), and acute respiratory distress syndrome (n = 1). Three children underwent retransplantation for acute graft failure (n = 2) or chronic rejection (n = 1). Pulmonary fibrosis was related to complications of treatment of acute of myelogenous leukemia with bone marrow transplantation in two children and to bronchiolitis obliterans, bronchopulmonary dysplasia, interstitial pneumonitis, and Langerhans cell histiocytosis in four others. Thirteen children underwent lung transplantation and concomitant cardiac repair. Bilateral lung transplantation, ventricular septal defect closure and pulmonary homograft reconstruction of the right ventricular outflow tract to the transplanted lungs was performed in three children by means of a new technique that avoids the need for combined heart-lung transplantation. Two patients had ventricular septal defect closure and single lung transplant for Eisenmenger's syndrome, two had ligation of a patent ductus arteriosus and transplantation, three additional children underwent atrial septal defect closure and lung transplantation, and two underwent lung transplantation for congenital pulmonary vein stenosis. Eight early deaths and three late deaths occurred (actuarial 1-year survival 62%). Lung transplantation in children has been associated with acceptable early results, although modification of the adult implantation technique has been necessary. Lung transplantation and repair of complex congenital heart defects is possible; heart-lung transplantation may only be required for patients with severe left heart dysfunction and associated pulmonary vascular disease. Bronchiolitis obliterans remains a major concern for long-term graft function in pediatric lung transplant recipients.

Cardiac asthma presenting as status asthmaticus: Deleterious effect of epinephrine therapy

Epinephrine is a potent bronchodilator currently used to treat severe asthma, although there is no proven advantage of this drug over beta 2 adrenergic agonists. By contrast, as demonstrated here, the use of such a potent vasoconstrictor can worsen hemodynamic status when left ventricular dysfunction is associated with asthma or is the cause for dyspnea. We describe the case of a 60-year-old man with an history of chronic asthmatic bronchitis admitted for status asthmaticus. Bronchodilator therapy, including high dosages of intravenous epinephrine, failed to improve the patient and he was intubated and mechanically ventilated. Several hours later, a right heart catheterization revealed severe unexpected left heart dysfunction with a capillary wedge pressure of 45 mmHg and a cardiac index of 1.7 l/min/m2. Epinephrine was gradually stopped which resulted in a decrease in mean arterial blood pressure and an improvement of hemodynamic status. He was discharged on home mechanical ventilation. In this patient, ischemic left heart failure was revealed by a clinical picture mimicking status asthmaticus. Epinephrine, given as bronchodilator therapy on an empiric basis precipitated the patient into cardiogenic shock. Therefore this drug should not be recommended in face of the possibility of cardiac asthma or associated cardiac dysfunction.

Predictability of left heart dysfunction from right heart performance--cardiac index-venous pressure plots and cardiac index-mean pulmonary artery wedge pressure plots at rest and their shift during dynamic exercise.

In an attempt to examine the extent to which the right heart performance can predict the left heart performance in heart diseases primarily affecting the left heart, we recorded cardiac index-venous pressure (CI-VP) plot and cardiac index-mean pulmonary artery wedge pressure (CI-PAW) plot at rest and investigated the shift of CI-VP plot and CI-PAW plot that occurred during mild dynamic exercise of the lower limbs. Six patients had normal heart function and 20 patients had heart diseases primarily affecting the left heart. The sensitivity, specificity, positive predictive value and negative predictive value in the estimation of the left heart function with delta CI/delta VP were 80%, 100%, 89% and 100%, respectively, when delta CI/delta PAW was regarded as the golden standard for the estimation of the left heart function. The sensitivity, specificity, positive predictive value and negative predictive value in estimating the left heart function with delta CI/delta RA were 86%, 93%, 92% and 86%, respectively. When the left heart function was estimated by delta VP alone without measuring delta CI, the sensitivity, specificity positive predictive value and negative predictive value were 40%, 100%, 73% and 100%, respectively. In short, it was possible to predict the left heart dysfunction with delta CI/delta VP or delta CI/delta RA, in the presence of the right heart dysfunction. It was also possible to predict a steep heart slope from normal delta CI/delta VP with error of 2/18 (11%), when steep left heart slope was predicted, based on the presence of steep right heart slope. In comparison, delta VP alone was a less sensitive index of the performance of the left heart.