Pilot assessment of the response of several pulmonary hemodynamic variables to sublingual sildenafil in candidates for heart transplantation

OBJECTIVE: To determine the acute vasodilator effect of sublingual sildenafil in heart transplant candidates with severe pulmonary hypertension due to severe left ventricular dysfunction (LVD). BACKGROUND: Pulmonary hypertension confers an increased risk of early graft failure. PATIENTS AND METHODS: Seven patients, (mean age of 53+/-8) with severe LVD (mean EF: 19+/-1.7%, functional class III-IV) due to coronary artery disease, dilated cardiomyopathy and valvulopathy were evaluated for heart transplant. All patients presented a mean transpulmonary gradient >12 mmHg and pulmonary vascular resistances >2.5 W.U., despite full treatment for advanced heart failure. The following hemodynamic data were obtained at basal state and then 15, 30 and 45 min after administration of 100 mg of sublingual sildenafil: right atrial, mean pulmonary artery pressure (mPAP), mean pulmonary capillary wedge pressures, mean transpulmonary gradient (mTPG), blood pressure, cardiac output, pulmonary vascular resistances (PVR) and systemic vascular resistances. Sublingual sildenafil was given without changing the previous treatment of heart failure. RESULTS: After 30 min of sublingual sildenafil, mPAP decreased from 37 (28-61) to 30 (16-42) mmHg and PVR decreased from 5.2 (1.9-13.8) to 2.5 (1.4-3.9) W.U. after 45 min. Mean TPG decreased from 19 (16-33) to 12 (8-14) mmHg at 45 min. Mean pulmonary capillary wedge pressure, cardiac output, systemic vascular resistances and mean blood pressure were unchanged. Sublingual sildenafil was well tolerated, with only transient facial flushing in 4 patients and mild headache in 2. CONCLUSIONS: Based on this initial study, sublingual sildenafil may be a useful alternative drug to perform acute vasodilator test in heart transplant candidates with significant pulmonary hypertension due to severe LVD. Nevertheless, further studies are warranted to confirm our results.     

A comparison of nesiritide vs. epoprostenol in a patient with precapillary pulmonary hypertension due to scleroderma complicated by postcapillary pulmonary hypertension

To the best of our knowledge, acute decompensated left-sided heart failure with preserved left ventricular ejection fraction in a patient with scleroderma has not been previously reported. We describe a patient with severe pulmonary hypertension due to limited scleroderma in whom nesiritide led to marked reductions in pulmonary arterial and capillary wedge pressure as well as resolution of symptoms and pulmonary edema. Subsequent epoprostenol use was associated with an increase in pulmonary capillary wedge pressure and a recurrence of pulmonary edema. Thus, nesiritide may be the preferred agent in scleroderma patients with severe pulmonary hypertension and preserved left ventricular systolic function since epoprostenol may lead to adverse hemodynamic effects.     

左心疾病相关肺动脉高压的临床诊治进展

左心疾病（ LHD）不仅是导致心力衰竭的临床常见疾病,也是临床常见的导致肺动脉高压（PH）的病因之一.临床流行病学研究提示,LHD相关PH是PH最常见疾病类型之一,PH是LHD患者预后重要的预测因素之一,合并PH的LHD患者预后不良.超声心动图检查是目前临床常用的筛查LHD相关PH的无创性检查方法,同时对于LHD相关PH患者的基础疾病的诊断与病情评估也具有重要作用.LHD相关PH患者典型的血流动力学改变特点为毛细血管后PH.对于疑似LHD相关PH患者进行包括肺毛细血管楔压（PCWP）、肺动脉压力（PAP）、肺血管阻力（PVR）以及跨肺压梯度（ mPAP - mPCWP）等血流动力学参数的血流动力学评估,具有重要的临床诊断、鉴别诊断、疾病评估和治疗决策作用.LHD相关PH的治疗首先应进行LHD基础疾病的优化治疗.虽然缺乏大型临床试验和循证医学的证据支持,治疗动脉型肺动脉高压有效的PH靶向治疗药物也被初步应用于部分LHD相关PH患者的治疗.LHD相关PH研究领域可能是目前及今后PH研究领域的热点和难点之一,也可能是目前及今后心力衰竭研究领域的热点之一.     

Natural history of primary pulmonary hypertension elucidated by pulmonary hemodynamics

The present study was undertaken to clarify the natural history of primary pulmonary hypertension (PPH) from a hemodynamic point of view. The subjects consisted of 83 patients (18 men and 65 women), whose ages ranged from 14 to 69 years and averaged 33 years. They were contacted through a nationwide survey. All patients underwent right-sided cardiac catheterization; cardiac output was measured in 52 patients and pulmonary capillary wedge pressure, in 40 patients. The following results were obtained. 1. The patients who died within three months of their cardiac catheterization were in severe right ventricular failure as shown by their elevated right atrial pressures and decreased cardiac indices. 2. The patients who died suddenly within two years of their cardiac catheterization had the same degree of right ventricular failure. The only difference was severe hypoxia in the patients with cardiac failure (54 +/- 21 vs 66 +/- 4 mmHg, p less than 0.05). 3. The patients who survived more than two years had normal right ventricular function. 4. Among the hemodynamic variables used to estimate prognosis; namely, pulmonary artery diastolic pressure, pulmonary capillary wedge pressure, cardiac index, pulmonary vascular resistance and pulmonary to systemic vascular resistance ratio, the cardiac index was the best predictor of prognosis.     

Discordance Between Clinical Assessment and Invasive Hemodynamics in Patients With Advanced Heart Failure

BackgroundHistorically, invasive hemodynamic guidance was not superior compared to clinical assessment in patients admitted with acute decompensated heart failure (ADHF). This study assessed the accuracy of clinical assessment vs invasive hemodynamics in patients with ADHF.Methods and ResultsWe conducted a prospective cohort study of patients admitted with ADHF. Prior to right-heart catheterization (RHC), physicians categorically predicted right atrial pressure, pulmonary capillary wedge pressure, cardiac index and hemodynamic profile (wet/dry, warm/cold) based on physical examination and clinical data evaluation (warm = cardiac index > 2.2 L/min/m²; wet = pulmonary capillary wedge pressure > 18 mmHg). We collected 218 surveys (of 83 cardiology fellows, 55 attending cardiologists, 45 residents, 35 interns) evaluating 97 patients. Of those patients, 46% were receiving inotropes prior to RHC. The positive and negative predictive values of clinical assessment compared to RHC for the cold and wet subgroups were 74.7% and 50.4%. The accuracy of categorical prediction was 43.6% for right atrial pressure, 34.4% for pulmonary capillary wedge pressure and 49.1% for cardiac index, and accuracy did not differ by clinician (P > 0.05 for all). Interprovider agreement was 44.4%. Therapeutic changes following RHC occurred in 71.1% overall (P < 0.001).ConclusionsClinical assessment of patients with advanced heart failure presenting with ADHF has low accuracy across all training levels, with exaggerated rates of misrecognition of the most high-risk patients.     

The Relationship of Pleural and Pericardial Effusion With Pulmonary Hemodynamics in Patients With Pulmonary Hypertension

BackgroundThe relationship between the presence of pleural and pericardial effusion in reference to hemodynamic parameters remains unclear in ambulatory patients with pulmonary hypertension (PH).MethodsConsecutive patients who underwent right catheterization (RHC) for the evaluation of pulmonary hypertension were enrolled. Point-of- care ultrasound was performed prior to the RHC to determine the presence of pleural effusion and pericardial effusion. We conducted a cross-sectional study to determine the association between presence of pericardial and pleural effusion with pulmonary hemodynamic variables.ResultsTwenty-five (78.1%) of 32 patients had evidence of PH by RHC. Mean pulmonary artery pressure of the population was 40.6 mmHg, and 68% (17/25) had WHO group I PH. Six (24.0%) of 25 PH patients had pleural effusions identified, of which 4 out of 6 (66.7%) had a pulmonary artery wedge pressure >15 mmHg. Eleven (44.0%) of the 25 PH patients were also found to have pericardial effusions, and most of those patients 10/11(90.9%) had an elevated right atrial pressure >10 mmHg. The presence of a pleural effusion was associated with a pulmonary artery wedge pressure >15 mmHg (p = 0.032) and the presence of a pericardial effusion was associated with a right atrial pressure >10 mmHg (p = 0.004). Detection of pleural effusion had a poor positive predictive value (67%) for the presence of pulmonary venous hypertension, whereas presence of a pericardial effusion was highly predictive (89%) of the presence of systemic venous hypertension.ConclusionsSystemic venous hypertension was associated with the presence of pericardial effusions, while pulmonary venous hypertension is associated with pleural effusion development in ambulatory patients with pulmonary hypertension.     

"Peak Summation" Left Ventricular Filling Pattern in Patients with Chronic Heart Failure

In patients with chronic heart failure (CHF) and a “peak summation” left ventricular pattern, no hemodynamic and prognostic information can be drawn from Doppler examination of mitral flow. In 263 consecutive patients with CHF who were undergoing simultaneous right heart catheterization and echo-Doppler examination, we prospectively determined (1) the frequency of the peak summation left ventricular filling pattern and (2) the incremental information contributed by pulmonary venous flow velocity patterns in providing noninvasive hemodynamic profile estimation. Isovolumic relaxation time of mitral flow, peak systolic (X), diastolic forward (Y), reverse (Z) flow velocity, and systolic fraction (X/X + Y) of pulmonary venous flow were measured. Forty-six of 263 (17%) patients had a peak summation left ventricular filling pattern. This subgroup showed more clinical deterioration (New York Heart Association functional class III-IV, 57% vs 49%; P < 0.01) and left atrial dysfunction (left atrial ejection fraction, 31% vs 39%; P < 0.001). However, 40% of these patients had a pulmonary wedge pressure of> 18 mmHg and a cardiac index of < 2.2 L/min/m². The systolic fraction of peak velocities of pulmonary venous flow showed a good correlation with pulmonary wedge pressure (r = -0.70, P < 0.05). The correlation was stronger in patients without mitral regurgitation (r = -0.81, P < 0.05). A systolic fraction of < 40% was accurate (sensitivity, 100%; specificity, 95%) in identifying patients with a pulmonary wedge pressure of < 18 mmHg. In patients without mitral regurgitation, this variable was also correlated with cardiac index (r = -0.65, P < 0.05) and predicted a cardiac index of < 2.2 L/min/m² (sensitivity, 91% specificity, 71%). In conclusion, a peak summation left ventricular filling pattern is common in patients with CHF. Pulmonary venous flow provides useful information about the hemodynamic profile of these patients.     

Hemodynamic effects of a combination of vasopressin and ketanserin in patients with hepatitis b-related cirrhosis.

We measured the hemodynamic effects of intravenous vasopressin, ketanserin (a 5-hydroxytryptamine-2 receptor blocker), and vasopressin plus ketanserin in 33 patients with hepatitis B-related cirrhosis. Thirteen patients received vasopressin alone (0.66 units/min), ten patients ketanserin alone (10 mg), and ten patients vasopressin followed by vasopressin plus ketanserin. Vasopressin alone reduced the hepatic venous pressure gradient (from 18 +/- 5, mean +/- S.D., to 9 +/- 3 mmHg, p less than 0.0001) and cardiac output (p less than 0.0001), but increased mean arterial pressure (p less than 0.005), mean pulmonary arterial pressure (p less than 0.0001), pulmonary capillary wedge pressure (p less than 0.0001), and systemic vascular resistance (p less than 0.001). There was no significant change in heart rate. Ketanserin alone produced a significant fall in the hepatic venous pressure gradient (from 16 +/- 4 to 13 +/- 3 mmHg, p less than 0.0001), mean arterial pressure (p less than 0.005), mean pulmonary arterial pressure (p less than 0.005), and pulmonary capillary wedge pressure (p less than 0.005). Heart rate, cardiac output, and systemic vascular resistance were not significantly changed. The addition of ketanserin to vasopressin corrected most of the systemic hemodynamic disturbances produced by vasopressin. This combination did not lead to a further reduction in the hepatic venous pressure gradient. We conclude that intravenous ketanserin reduces portal pressure in patients with hepatitis B-related cirrhosis. The addition of ketanserin to vasopressin improves the detrimental systemic hemodynamic effects of vasopressin without further reducing the portal pressure.     

肺动脉高压的诊断和评估

肺动脉高压（pulmonary hypertension，PH）评估的目的是确定疾病的严重程度、血液动力学病变的本质和后果、病因诊断及伴随的症状。对有临床症状和胸部X线提示PH表现者，要详细地询问病史和细致的体检，而对病因和严重程度的评估可通过超声心动图、能气／血流扫描、胸部CT、肺功能检查、夜间血氧监测来完成。对超声心动图显示中度至严重PH和准备实施治疗者，要进行右心导管插管测定肺动脉压力。对处于发生PH危险因素的患者，要给予超声心动和肺功能检查，从而对PH的发展和预后进行评估。不推荐用基因检测对原发性PH常规评估。     

Heart rate variability in severe right or left heart failure: the role of pulmonary hypertension and resistances

BACKGROUND: The decrease in heart rate variability (HRV) might be related to the hemodynamic status in heart failure. However, HRV in patients with severe isolated right heart failure has not been extensively studied. AIMS: This study compared HRV in patients with congestive heart failure (CHF) and in patients with isolated right heart failure. METHODS: Time and frequency domain analysis of HRV on 24-h ECG recording was assessed in 15 healthy subjects and in two groups of patients with severe heart failure awaiting heart or heart/lung transplantation. These were 15 patients with CHF due to idiopathic dilated cardiomyopathy (IDC) and 10 patients with isolated right heart failure due to primary pulmonary hypertension (PPH). RESULTS: Measurement of HRV were significantly decreased in both groups of patients compared with the control group. Patients with IDC had higher pulmonary capillary wedge pressure than patients with PPH (P=0.04) but lower pulmonary artery pressure and lower pulmonary vascular resistance (PVR) (P<0.0001). However, all the measurements of HRV were significantly lower in patients with IDC than in patients with PPH (range 22-77%, P<0.05 to P<0.01). None of the HRV measurements correlated with filling pressure measurements. CONCLUSIONS: The increase in pulmonary vascular resistance in heart failure is not the main causal factor behind a decrease in HRV.     

Pulmonary Hypertension in Advanced Heart Failure

Abstract The diagnosis of pulmonary hypertension is easy during routine evaluation of patients with chronic heart failure by means of Doppler echocardiography. However, one must remember that an accurate hemodynamic characterization of the pulmonary circulation requires right heart catheterization to measure pulmonary vascular resistance and, if necessary, to test the reversibility of pulmonary hypertension. In addition, the importance of combining the right heart hemodynamic variables with a functional evaluation of the right ventricle is emphasized: in fact, the clinical impact of pulmonary hypertension in advanced heart failure patients (in terms of both exercise intolerance and prognosis) seems to be modulated by right ventricular function.     

Effects of omapatrilat on hemodynamics and safety in patients with heart failure

Omapatrilat, a novel vasopeptidase inhibitor, is a highly potent and selective inhibitor of neutral endopeptidase and angiotensin-converting enzyme; its therapeutic potential is being investigated for treatment of hypertension and heart failure. In the present study, the safety, tolerability, and hemodynamic effects of single oral doses of omapatrilat (1 to 50 mg) are compared with placebo in patients with heart failure. Patients with heart failure (New York Heart Association functional class II to IV) and a resting left ventricular ejection fraction < or = 40% were enrolled in a double-blind, placebo-controlled, sequential-panel study of single doses of omapatrilat of 1, 2.5, 5, 10, 25, or 50 mg, followed by hemodynamic assessment for 24 hours. At 4 to 6 hours after dosing, the 25- and 50-mg doses of omapatrilat, compared with placebo, reduced mean pulmonary capillary wedge pressure by approximately 6 mm Hg from 20 and 23 mm Hg at baseline to 14 and 16 mm Hg. The 50-mg omapatrilat dose maintained this effect compared with placebo with an approximately 2.5-mm Hg reduction in mean pulmonary capillary wedge pressure at 24 hours. Omapatrilat improved additional hemodynamic parameters, including cardiac index, systemic vascular resistance, stroke volume index, and mean arterial pressure. Additionally, by 2 hours after dosing with omapatrilat 25 and 50 mg, a trend in peak increases from baseline in plasma atrial natriuretic peptide (twofold) and cyclic guanosine monophosphate (nearly twofold) was observed. Moreover, omapatrilat was well tolerated. Thus, omapatrilat administered orally to patients with heart failure was safe and well tolerated and resulted in improved hemodynamic performance.     

Sinus node inhibitors in coronary surgery

In patients with coronary artery disease, rapid ventricular rates require adequate treatment since disturbed oxygen balance and ischemia may be incurred. By virtue of their isolated action on the sinus node, "specific bradycardic substances" have only negligible hemodynamic side effects and, accordingly, represent an alternative to other available rate-slowing drugs. The clonidine derivative, alinidine (N-allyl-clonidine) was used primarily as the specific bradycardic substance in our studies in patients at the time of aortocoronary bypass surgery. In addition to its rate-slowing properties, this substance also elicits an analgetic and anti-ischemic effect and, in a small percentage, it is metabolized to clonidine. The purpose of this study was to assess the effectiveness and hemodynamic actions of alinidine in the treatment of intraoperative heart rate acceleration and, in combination with the calcium channel blocker nifedipine, to evaluate its use for postoperative hypertension. The first study was performed in nine patients in whom, during aortocoronary bypass surgery, there was a heart rate increase in excess of 20% above the preoperative control value. Patients were excluded with impaired ventricular function, absence of sinus rhythm, concomitant increase in arterial mean pressure greater than 30%, hypovolemia, pulmonary capillary wedge pressure in excess of 15 mmHg as well as those with ECG changes precluding exact assessment of myocardial ischemia. In addition to the ECG, the following parameters were registered: heart rate, arterial pressure, central venous pressure and, with a semi-floating balloon-tipped catheter, pulmonary artery pressure as well as pulmonary wedge pressure. Cardiac output was determined with thermodilution.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transthoracic echocardiographic parameters in the estimation of pulmonary capillary wedge pressure in patients with present or previous heart failure

Multiple echocardiographic criteria are routinely used for the estimation of left heart filling pressures. We assessed the predictive value of various echocardiographic parameters to estimate the left heart filling pressure and proposed a simplified approach for its evaluation. We collected the clinical, echocardiographic, and invasive hemodynamic data from 93 patients with heart failure who underwent right-sided heart catheterization and transthoracic echocardiography within a 24-hour period. Of these 93 patients, 57% had a left ventricular ejection fraction <50% and 69% had an elevated mean pulmonary capillary wedge pressure of ≥15 mm Hg. A mitral E/E' of ≥15 had a sensitivity of 55% but a specificity of 96%. A left atrial area of ≥20 cm(2) had a sensitivity of 66% and specificity of 89%. A deceleration time <140 ms had a sensitivity of 51% and specificity of 93% to predict a pulmonary capillary wedge pressure of ≥15 mm Hg. The combination of E/E' ≥15 ± left atrial area of ≥20 cm(2) ± deceleration time <140 ms provided a sensitivity of 92% and specificity of 85%. On multivariate analysis, the combination of E/E' ≥15, left atrial area of ≥20 cm(2), and deceleration time <140 ms was the most significant predictor of a pulmonary capillary wedge pressure of ≥15 mm Hg (odds ratio 48, 95% confidence interval 10 to 289, p <0.001). In conclusion, this simplified approach using 3 echocardiographic parameters provides an accurate and a practical approach for the routine estimation of the elevated left heart filling pressure.     

Relation between hemodynamic and ventilatory responses in determining exercise capacity in severe congestive heart failure

The cause of exercise intolerance in congestive heart failure is unclear. Hemodynamic and ventilatory responses were measured during symptomatic maximal upright bicycle exercise in 28 patients with chronic severe left ventricular failure who achieved a maximal oxygen uptake of only 12 +/- 4 ml/min/kg (+/- standard deviation). All patients reached anaerobic metabolism as the respiratory exchange ratio rose and arterial pH fell significantly. Pulmonary capillary wedge pressure increased from 20 +/- 10 mm Hg at rest to 38 +/- 9 mm Hg at peak exercise and cardiac index increased from 2.51 +/- 0.73 to 4.54 +/- 1.65 liters/min/m2 (both p less than 0.001). Systemic vascular resistance decreased, but pulmonary vascular resistance did not change during exercise. Despite the marked pulmonary venous hypertension at peak exercise, blood gases were unchanged (PaO2, 96 +/- 15 mm Hg; PaCO2, 35 +/- 7 mm Hg). Systemic arterial oxygen content increased from 16 +/- 2 to 17 +/- 2 vol% (p less than 0.01). Changes in pulmonary capillary wedge pressure did not correlate with changes in arterial oxygen content. Results were similar whether patients were limited by dyspnea or fatigue. Thus, exercise intolerance in patients with severe left ventricular failure is associated with marked elevation of pulmonary capillary wedge pressure and anaerobic metabolism without hypoxemia or altered carbon dioxide tension. These findings suggest that exercise ability in congestive heart failure is more dependent on cardiac output than on ventilatory consequences of pulmonary congestion.     

Right ventricular cardiomyopathy in beta-thalassaemia major.

AIMS: To evaluate right ventricular function in patients with beta-thalassaemia major and congestive heart failure.Background In patients with beta-thalassaemia major a high incidence of cardiac involvement still exists despite improved prognosis with chelation therapy. Development of severe right heart failure is common and has been attributed to pulmonary hypertension secondary to lung haemochromatosis. However, the possibility of direct right ventricular myocardial involvement in the absence of significant pulmonary hypertension has not been adequately investigated. METHODS: Twenty-nine consecutively screened patients with beta-thalassaemia major and congestive heart failure were investigated by Doppler echocardiography, right ventricular first-pass radionuclide examination and cardiac catheterization. Haemodynamic data were obtained both before and after volume loading. A control group of 39 patients with beta-thalassaemia major, free from cardiac disease, and matched for age, gender, body surface area and heart rate was used for comparison. A subset of the control thalassaemic group (n=15) underwent both radionuclide and haemodynamic assessment. RESULTS: The majority of patients were on non-optimal chelation therapy. Only two of 29 patients were found to have cor pulmonale. One other patient suffered from constrictive pericarditis. A restrictive filling pattern in both ventricles and left ventricular systolic dysfunction were evident in the other 26 patients. Pulmonary artery pressure (systolic, 33+/-8 vs 27+/-5 mmHg, P<0.05) and pulmonary vascular resistance (114+/-56 vs 65+/-29 dynes. s. cm(-5), P<0.01) were only mildly elevated in the heart failure group. After volume challenge, cardiac output remained unchanged although the increments of ventricular filling pressures were significant (Deltaright atrial: 4.8+/-2.2 mmHg, P<0.05; Deltapulmonary capillary wedge: 5.6+/-2.9 mmHg, P<0.05) and correlated with each other (r=0.69;P<0.001) in heart failure patients, suggesting pericardial constraint and ventricular interaction. In these patients compared with the control thalassaemic group, a lower right ventricular ejection fraction (29%+/-9 vs 59%+/-6, P<0.0001) without correlation with pulmonary artery pressures was found. Haemodynamically significant right ventricular dysfunction defined as mean right atrial pressure >10 mmHg and ratio of mean right atrial-to-capillary wedge pressure >0.8 was evident in 15 of the 26 patients (58%), all with severe symptoms, representing three fourths of the patients in functional class III and IV. Simultaneous pressure recordings in six of these 15 patients showed equalization of ventricular end-diastolic pressures within 5 mmHg. CONCLUSION: The majority of patients with beta-thalassaemia major and severe congestive heart failure demonstrated a unique haemodynamic pattern similar to that described in predominant right ventricular infarction, indicating severe right ventricular cardiomyopathy in addition to left ventricular dysfunction. The incidence of cor pulmonale as a cause of right heart failure seems to be much lower than previously hypothesized.     

The pressure-flow response of the pulmonary circulation in patients with heart failure and pulmonary vascular disease

Although it is well known that the pulmonary circulation is altered in patients with pulmonary arterial or venous hypertension, the resultant hemodynamic behavior has not been systematically studied. We undertook to do so in a group of patients with pulmonary hypertension of diverse etiology. We measured pulmonary arterial (PAP) and occlusive wedge pressures and cardiac output at rest (i.e., standing) and during progressive upright treadmill exercise in 51 patients. Forty-two had chronic, stable, cardiac failure secondary to ischemic, myopathic or valvular heart disease and were grouped according to whether their mean PAP was less than (normotensive) or greater than (hypertensive) 19 mm Hg, and nine had pulmonary vascular disease of diverse etiology and were considered separately. In the majority of patients, we found that irrespective of whether the hypertension was arterial or venous in origin or etiology: the mean PAP-flow relationship was linear; pulmonary capillary wedge pressure was greater than or equal to the average closure pressure of the pulmonary vascular bed and could therefore be used as the downstream pressure in calculating pulmonary vascular resistance; and pulmonary vascular resistance declined with exercise. Notable exceptions to the third observation were patients with valvular heart disease or a resting pulmonary vascular resistance greater than 800 dyne-sec-cm-5.     

Identification of high risk subsets of acute myocardial infarction. Derived from the myocardial infarction research units cooperative study data bank

To Identify the patient at high risk after acute myocardial Infarction data on 400 patients obtained from the Myocardial Infarction Research Units Cooperative Data Bank were examined. Patients were grouped according to clinical findings as follows: uncomplicated (class 1, 81 patients); mild to moderate failure (class II, 150 patients); severe failure with pulmonary edema (class III, 17 patients); and severe failure with shock (class IV, 152 patients). Hemodynamic data Including pulmonary capillary wedge pressure and cardiac output were available In all patients. High risk subsets within clinical classes I, II and IV were Identifiable. In class I, nonsurvivors had significantly (P <0.05) higher values for pulmonary capillary wedge pressure (16 mm Hg) and heart rate (96 beats/min); nonsurvivors In class II also had a significant (P <0.01) elevation In pulmonary capillary wedge pressure (23 mm Hg); and In class IV the high risk subset was characterized (P <0.01) by pulmonary capillary wedge pressure (21 mm Hg), heart rate (100 beats/min), cardiac Index (1.6 liters/min per m²), stroke index (14 cc/m²) and stroke work index (12 g-m/m²). Discrimlnant function analysis using pulmonary capillary wedge pressure and heart rate predicted mortality In classes I to III with 72 percent accuracy; a similar equation representing stroke work index, pulmonary capillary wedge pressure and cardiac Index had an 83 percent rate of accuracy in class IV patients. interclass comparison of the last three measurements indicated that the data differed significantly among classes, thus signifying a spectrum of ventricular impairment after Infarction that was commensurate with the clinical presentation. However, in individual patients the clinical examination did not consistently reflect the degree of ventricular dysfunction. Thus, careful bedside examination together with hemodynamic monitoring of wedge pressure, cardiac output and heart rate serve to identify the high risk patient after acute myocardial infarction.     

Findings on routine right heart catheterization in patients with suspected coronary artery disease

Whether catheterization of the right heart should be performed routinely in all patients undergoing coronary angiography for assessment of coronary artery disease is controversial. To objectively assess the utility of routine right heart catheterization, hemodynamic data from 2,178 patients studied for angina having no signs, symptoms, or history of congestive heart failure were analyzed retrospectively. The salient results are as follows: 0.9% patients had unsuspected mitral valve gradients greater than or equal to 5 mm Hg; 0.4% had occult left-to-right shunts; 1% had pulmonary hypertension (pulmonary artery systolic pressure greater than or equal to 40 mm Hg) not attributable to an elevated mean pulmonary capillary wedge pressure (PCWP); 4.8% had PCWP greater than or equal to 18 mm Hg; 6% had cardiac indexes less than or equal to 2.0 L/min/m2, suggesting subclinical left ventricular failure. Overall, 14.5% of patients had at least one abnormal right-sided hemodynamic variable revealed by right heart catheterization. The frequency of abnormalities increased with increasing Canadian Cardiovascular Society grade of angina. Ten percent of grade 1, 14% of grade 2, 15% of grade 3, and 19% of patient 4 patients had at least one abnormality (phi 2 test, p less than or equal to 0.005). It is concluded that the right heart catheterization adds an important dimension to the diagnosis and treatment of patients undergoing coronary angiography for assessment of coronary artery disease and might significantly influence subsequent patient management.     

Effects of positive end-expiratory pressure ventilation and extracorporeal ultrafiltration method in patients with refractory heart failure

We studied the effects of positive end-expiratory pressure (PEEP) ventilation in ten patients with acute myocardial infarction (nine in Killip class III, one in Killip class IV; pulmonary capillary wedge pressure greater than 24 mmHg) and of extracorporeal ultrafiltration method (ECUM) in seven patients with refractory heart failure due to acute myocardial infarction and others. Application of PEEP resulted in significant increases in PaO2 and SaO2 and decrease in PaCO2. Significant reduction in mean pulmonary arterial and pulmonary capillary wedge pressures and heart rate was observed, while stroke work index increased significantly. There was a significant correlation between changes in stroke work index and PaO2 after the application of PEEP. The use of ECUM removed fluid of 1416 +/- 662 ml (680-2800 ml) with the ultrafiltration flux rate being 478 +/- 223 ml/hour. Significant decreases in mean pulmonary arterial, pulmonary capillary wedge and central venous pressures were observed, while PaO2 increased significantly. BUN and serum creatinine levels increased significantly, and total protein and serum albumin tended to increase. There was a significant correlation between fluid removed and change in PaO2 after the use of ECUM. Thus, PEEP and ECUM are beneficial for patients with refractory heart failure. The mechanism(s) are: reduction in preload due to an increased intrathoracic pressure and a decreased systemic venous return with PEEP, or due to removal of excess fluid with ECUM, and improvement of the oxygenation of the blood.