Degree Of Congestive Heart Failure Research Articles

Electrolyte Imbalance Caused by Diuretic Therapy in Infants with Congenital Heart Diseases

Background: Although furosemide and spironolactone are widely used to treat heart failure in infants and children because of their effectiveness and few side effects, there have been no prospective studies about the frequency and degree of serum electrolyte abnormality after the use of diuretics in pediatric patients. Methods: We prospectively studied 126 infants at our outpatient clinic aged less than 2 months old with left-toright shunt who received oral diuretics. All patients were started on furosemide at 0.5~3 mg/kg/day and spironolactone at 0.5~2 mg/kg/day, orally divided into two or three doses according to the degree of congestive heart failure. Results: Serum sodium level ranged from 128 to 142 mEq/L (mean 136 mEq/L) and was 6.0 mEq/L) was complicated in 19 patients. Eighteen patients with sodium levels of <134 mEq/L after diuretics showed lower body weight at the start of diuretics and lower postnatal age than the patients with serum sodium levels ≥ 134 mEq/L. Conclusion: Although neither severe hyponatremia nor hypokalemia developed, there were a few patients with prolonged hyponatremia after diuretic therapy. It seems to be preferable to monitor serum electrolyte levels carefully after the start of diuretic therapy in infants with congenital heart disease.

182 To Admit or Discharge Congestive Heart Failure Patients: Use of a Severity of Illness Index

182 To Admit or Discharge Congestive Heart Failure Patients: Use of a Severity of Illness Index

Sudden Cardiac Death Risk Prediction

Sudden Cardiac Death Risk Prediction

Predictive factors for the severity of congestive heart failure after an epirubicin-based treatment for metastatic breast cancer.

1124 Background: Patients treated with anthracyclines have a well described risk for developing congestive heart failure (CHF). However, little is known about possible predictive factors for the severity of the CHF acquired. Methods: 125 patients who developed CHF class ≥ II according to New York Heart Association (NYHA) guidelines were included in this retrospective study. The patients were recruited consecutively from 1,097 patients with metastatic breast cancer admitted to Herlev Hospital from November 1983 through November 2003 for an epirubicin-based chemotherapy. No patients treated had a history of cardiac disease before start of epirubicin. Statistics: Univariate analysis based on ordinal logistic regression with NYHA class at time of cardiac disease as the outcome. Results: The median time after cessation of epirubicin to onset of CHF was 3 months (range 0.01 to 66.7 months). The median survival was 7.3 months (range 0.01 to +121.1 months), with eights patients (6.4%) still alive. The distribution of patients in the NYHA class II, III, IV and class ≥ II was: 35 patients (28%), 38 patients (30.4%), 39 patients (31.2%), and 13 patients (10.4%), respectively. Following variables were tested in the univariate analysis: cumulative dose of epirubicin mg/m2, age at the time of epirubicin treatment, previous antihormonal treatment or mediastinal irradiation, and comorbidity with disposition to heart disease. Variables there all previously had been demonstrated as a risk factor for developing CHF after an epirubicin treatment. Moreover, the time from the cessation of epirubicin treatment to the onset of cardiotoxicity and the value of serum-lactatdehydrogenase at the onset of the CHF were included. None of these variables became significant, even at a level of 0.20. Conclusions: No predictive factor for the degree of congestive heart failure (NYHA class) was identified in patients with heart failure due to an epirubicin treatment. Even cumulative epirubicin dose mg/m2, age, comorbidity with disposition to heart disease, or previous mediastinal irradiation had an influence of its own. No significant financial relationships to disclose.

A Review of the Association Between Congestive Heart Failure and Cognitive Impairment

Heart failure is a growing epidemic with an estimated 5 million Americans suffering from this condition. Several clinical trials have demonstrated a high correlation between congestive heart failure (CHF) and cognitive impairment. The severity of cognitive impairment correlates positively with the degree of CHF. The underlying mechanism for cognitive impairment remains unclear but appears to be related to cerebral hypoperfusion and impaired cerebral reactivity with selective impairment of verbal memory and attention domains. Furthermore, cognitive dysfunction represents one aspect of frailty, a novel concept that encompasses a range of clinical conditions that results in functional impairment in patients with heart failure. In addition, frailty independently predicts mortality in CHF patients. Cognitive impairment is a common and predictable effect of CHF that contributes with social and behavioral problems to decreased compliance to prescribed therapy and increased hospital readmissions. A multidisciplinary approach is necessary to deal with the complexity of this clinical syndrome.

Does digoxin improve the prenatal outcome of the fetus with congestive heart failure in sinus rhythm?

TIVE HEART FAILURE IN SINUS RHYTHM? JAMES HUHTA, BETTINA CUNEO, JENNY LESHKO, RICHARD MARTINEZ, University of South Florida, Pediatrics, St. Petersburg, Florida, Rush University Medical Center, Pediatrics, Chicago, Illinois OBJECTIVE: Show that digoxin therapy in the prehydropic fetus in sinus rhythm could limit progression of congestive heart failure (CHF) and thereby prolong gestation thus improving prenatal outcome. STUDY DESIGN: We reviewed the clinical course and outcomes of 12 fetuses presenting between 24-32 weeks with CHF and sinus rhythm treated with digoxin. Degree of CHF was assessed by two methods: a 10 point cardiovascular profile score (CVPS) (measured in all fetuses) derived from echo Doppler findings of cardiomegaly, depressed systolic shortening, AV valve insufficiency, abnormal diastolic compliance, and hydrops; and ventricular Tei index (measured in 5 fetuses). Four fetuses had aortic obstruction secondary to valve stenosis or large rhabdomyoma, 2 had right sided abnormalities (TOF with absent pulmonary valve and critical PS), 2 had cardiomyopathy, and 4 had structurally normal hearts with high output CHF due to twin to twin transfusion (2), acardiac twin or sacrococcygeal teratoma. Transplacental digoxin (loading dose of 0.5 mg IV q8 ! 3) followed by maintenance doses of 0.25 to 0.375 q 12 hr were given to maintain therapeutic levels of 0.9-1.8 ng/ml for 3-12 weeks. RESULTS: Nine infants were delivered alive at 28-36 (mean 32) weeks; 7 survived hospital stay. CHF progressed despite digoxin in 3/3 hydropic fetuses. Two hydropic fetuses and one nonhydropic fetus died in utero. Of 9 fetuses initially responding to digoxin, CVS remained stable in 3, improved in 4, and transiently improved then worsened in 2. The most immediate improvements were in ventricular shortening. Tei index did not correlate with CVPS, and improved in 2, worsened in 2 and did not change in 1. CONCLUSION: Digoxin appears to limit the progression of CHF and prolong gestation in fetuses with sinus rhythm with an abnormal CVPS due to CHD or noncardiac malformations, but is ineffective once hydrops has developed. We speculate that the improvements in ventricular function with digoxin may result from decreased systemic vascular resistance.

Heart failure complicated by atrial fibrillation: mechanistic, prognostic, and therapeutic implications.

Atrial fibrillation and congestive heart failure are two distinct clinical entities that are responsible for significant morbidity and mortality in the Western world. Hypertension, coronary artery disease, and nonischemic cardiomyopathy represent the most prevalent underlying pathologies of both diseases, implying a coincidence of both in many patients. The prevalence of atrial fibrillation with a progressive degree of congestive heart failure is increasing, as judged by New York Heart Association functional class. Moreover, the presence of congestive heart failure has been identified as one of the most powerful independent predictors of atrial fibrillation, with a sixfold increase in relative risk of its development. On the other hand, atrial fibrillation can cause or significantly aggravate symptoms of congestive heart failure in previously asymptomatic or well-compensated patients. In some patients, symptomatic dilated cardiomyopathy may develop over time entirely due to atrial fibrillation with rapid ventricular rates. Upon restoration of sinus rhythm, this type of "tachymyopathy" has been shown to be often reversible. Recent investigations of the physiologic and structural changes of the atrial myocardium ("electrical and structural remodeling") have shown that neurohumoral activation, fibrosis, and apoptosis are demonstrable with both diseases. On the other hand, experimental data suggest that the substrates of atrial fibrillation in congestive heart failure are different from those of pure atrial tachycardia-related forms of atrial fibrillation. This review highlights the clinical and pathophysiologic similarities and differences of atrial fibrillation and congestive heart failure relevant to the understanding, treatment, and prevention of these diseases in the population at risk.

Congenital heart disease and acquired valvular lesions in pregnancy

Hintergrund: Die jahrliche Zahl schwangerer Herzfehlerpatientinnen betragt in Deutschland etwa 6 000 (jede 130. Schwangerschaft). Die voraussehbaren hamodynamischen Veranderungen in der Schwangerschaft erlauben in der Mehrzahl der Falle eine recht zuverlassige Vorhersage des Schwangerschaftsverlaufs fur Mutter und Kind. Folgende funf Aspekte sind von betrachtlicher klinischer Bedeutung. Unkorrigierte angeborene Herzfehler: Patientinnen mit nicht korrigierbaren komplexen Herzfehlern, einer nach Palliationsoperation persistierenden myokardialen Insuffizienz oder betrachtlichen pulmonalvaskularen Widerstandserhohungen sollte von einer Schwangerschaft abgeraten werden. Pratrikuspidale Kurzschlussverbindungen werden in der Schwangerschaft in aller Regel gut toleriert. In den seltenen Fallen einer deutlichen symptomatischen Verschlechterung ist der katheterinterventive Shuntverschluss heute Therapie der Wahl. Bei Patientinnen mit Ventrikelseptumdefekt oder persistierendem Ductus Botalli liegt in aller Regel ein flussbegrenzender Defekt vor, der sich im Verlauf einer Schwangerschaft meist nicht negativ auswirkt. Bei unbehandelten Aortenisthmusstenosen sind in 2,3% der Falle schwere Hypertonien, myokardiale Dekompensationen, Aortendissektionen und zerebrale Blutungen berichtet worden, deren Pravention spezifische Beratung und Therapie erfordert. Korrigierte angeborene Herzfehler: Die Gefahrdung von Mutter und Kind ist nach Korrekturoperationen einer Fallot'schen Tetralogie vom Korrekturergebnis abhangig. Das Risiko erscheint gut abschatzbar. Bei komplexen zyanotischen Vitien besteht ein deutlich erhohtes maternales Risiko bezuglich myokardialen Pumpversagens, thromboembolischer Komplikationen, komplexer Arrhythmien und Endokarditiden. Die Inzidenz fetaler Aborte, Fruhgeburten, Unreife bei der Geburt sowie kongenitaler Fehlbildungen betragt > 50%. Erworbene Herzklappenfehler: Aufgrund der Schwangerschaftsphysiologie verschlechtert sich die hamodynamische Situation bei Mitralstenosen regelhaft. Patientinnen mit Klappenoffnungsflachen < 1,5 cm2 tolerieren diese Schwangerschaftsbedingungen haufig nicht. Sind die begrenzten Moglichkeiten einer medikamentosen Therapie erschopft, ist die perkutane Ballonvalvulotomie heute Therapie der Wahl. Die in Kompetenzzentren erzielten Behandlungsergebnisse sind auserordentlich gunstig. Die schwangerschaftstypische periphere Vasodilatation und Frequenzerhohung fuhren dazu, dass die hamodynamischen Auswirkungen einer Mitral- und Aorteninsuffizienz wahrend der Schwangerschaft in aller Regel nicht aggraviert werden. Aortenklappenstenosen sind bei Schwangeren auserordentlich selten. Der transaortale Blutfluss und Gradient nehmen im Verlauf der Schwangerschaft aufgrund der relativ verlangerten Systolendauer ab. Die linksventrikulare Wandspannung nimmt dagegen zu, so dass trotz Abnahme des Gradienten eine myokardiale Dekompensation resultieren kann. Hypertrophe Kardiomyopathie: Der Verlauf gestaltet sich meist gunstig. Eine praexistente Herzinsuffizienz wird bei etwa 20% der Patientinnen in der Schwangerschaft aggraviert. Besonders schlecht toleriert werden Vorhofflimmerepisoden und supraventrikulare Tachykardien. Beide konnen Mutter und Fetus gefahrden. Orale Antikoagulation: Die moglichen Antikoagulationsstrategien sind mit einem unterschiedlich hohen maternalen und fetalen Risiko verbunden. Bei gegebener Indikation ist die ununterbrochene orale Antikoagulation mit Phenprocoumon mit dem geringsten Risiko fur die Mutter, die Beendigung jeglicher Antikoagulation mit dem geringsten Risiko fur das ungeborene Kind verbunden. Einzelentscheidungen sind schwierig und sollten in die Hand eines erfahrenen Kompetenzzentrums gegeben werden.

CXC-chemokines, a new group of cytokines in congestive heart failure--possible role of platelets and monocytes.

The purpose of the present study was to examine the circulating levels of CXC-chemokines in patients with various degree of congestive heart failure (CHF). CXC-chemokines may be important mediators in the persistent immune activation observed in CHF patients by activation of circulating neutrophils, T-cells and monocytes and possibly by the recruitment of these cells into the failing myocardium. Levels of interleukin (IL)-8, growth-regulated oncogene (GRO) alpha and epithelial neutrophil activating peptide (ENA)-78 were measured both in serum and in platelet-free plasma by enzyme immunoassay in 47 patients with CHF and in 20 healthy controls. (i) CHF patients had significantly elevated levels of all the three CXC-chemokines with IL-8 and GRO alpha showing a gradual increase along with increasing NYHA class. (ii) There was an inverse correlation between IL-8 and left ventricular ejection fraction (EF) and cardiac index (CI). (iii) Both unstimulated and lipopolysaccharide (LPS)-stimulated monocytes from CHF patients released markedly elevated amounts of all three CXC-chemokines. (iv) Platelets from patients with severe CHF were characterised by decreased content of GRO alpha and ENA-78 as well as decreased release of these chemokines upon thrombin receptor stimulation. (v) Activated platelets stimulated peripheral blood mononuclear cells in vitro to enhanced release of IL-8, and neutralising antibodies against ENA-78 inhibited this interaction. This study demonstrates for the first time elevated levels of CXC-chemokines in CHF, which may be of importance for progression of heart failure. Our findings further suggest that activated monocytes and platelets may contribute to enhanced CXC-chemokine levels in CHF.

Nursing management of congestive heart failure. Part I.

Congestive heart failure (CHF) is a common clinical problem and in its advanced stage has a poor prognosis. Approximately 400,000 individuals develop heart failure each year (Parmley 1989). CHF can be caused by coronary artery disease such as myocardial infarction, ischemia and hypertension. Should heart failure occur as a result of acute myocardial infarction, a classification tool developed by Killip can be used to assess the degree of CHF. Killip's classification is organised into the following four categories: Class I: no heart failure Class II: mild to moderate failure Class III: acute pulmonary oedema Class IV: cardiogenic shock (Killip, as cited by Benz 1989). This system helps in organising clinical signs and symptoms of heart failure. Due to the fact that CHF is now the most common hospital discharge diagnosis for those over the age of 65, critical care nurses need to be able to recognise complications and intervene rapidly (Parmley 1989) in collaboration with medical staff. The purpose of this paper is first to discuss cardinal signs and symptoms and clinical data associated with CHF. Second, critical care nurses' management of CHF is organised around common nursing diagnoses.

Nitroglycerin-Induced Heparin Resistance: Absence of Interaction at Clinically Relevant Doses

A diminution in the anticoagulant effect of IV heparin with concomitant use of IV nitroglycerin has been reported. However, recent reports have disputed the existence of this interaction. The objective of this study was to assess the potential interaction of these agents in a clinical setting. Forty-five patients hospitalized with angina or acute myocardial infarction received low-dose nitroglycerin (5-20 micrograms/minute), and 13 received high-dose nitroglycerin (80-240 micrograms/minute). The two groups were similar with respect to sex, age, weight, and angina class; however, the high-dose group had a greater degree of congestive heart failure. The heparin dose required to achieve therapeutic anticoagulation did not differ between the groups. Results suggest no inhibition of heparin anticoagulation by IV nitroglycerin at clinically relevant doses.

Neurohumoral activation in congestive heart failure

This article reviews the evidence that congestive heart failure is accompanied by an increased plasma norepinephrine concentration and that this is due not only to a reduced tissue clearance of the substance but also to a marked increase in sympathetic nerve activity. It also reports data that indicate that the sympathetic activation is associated with an activation of the renin-angiotensin system and an increased plasma level of vasopressin. At which degree of congestive heart failure these phenomena become manifest is not clear, but some studies suggest that the sympathetic and renin-angiotensin systems may be normal in asymptomatic congestive heart failure but already somewhat activated when this condition reaches New York Heart Association class II. There is also evidence that this activation, though initially compensatory, is eventually responsible for a number of adverse cardiovascular effects that account for the negative relationship between this event and survival. Finally, the article discusses the inability of the increased plasma level of atrial natriuretic peptide that characterizes congestive heart failure to offset the adverse effects of the neurohumoral activation and the variable influence of drug treatment on this phenomenon. This is not impossible to achieve, however, because heart transplantation appears to rapidly normalize a major factor in the increased sympathetic activity observed before surgical intervention, that is, impairment of the arterial baroreflex.

Urinary cyclic guanosine monophosphate as an indicator of experimental congestive heart failure in rats

STUDY OBJECTIVE--The aim was to investigate the relationship between urinary cyclic guanosine monophosphate (GMP) excretion and activation of the heart endocrine function in two rat models of cardiac failure. DESIGN--Left ventricular infarction and aging in spontaneously hypertensive rats (SHR) are two models that could lead to congestive heart failure. In the first the degree of failure depends on the length of the infarcted area. In the second the degree of failure depends on time. Urinary cyclic GMP, plasma atrial natriuretic factor (ANF), and degree of congestive heart failure were evaluated in both models. EXPERIMENTAL ANIMALS--31 male Wistar rats were used for myocardial infarction and sham operated controls. Spontaneously hypertensive (SHR) rats (2, 6, 12 and 24 months old, n = 10 per group) were used for the age overload studies. MEASUREMENTS AND MAIN RESULTS--In myocardial infarction, the amount of left ventricular ANF mRNA, plasma ANF concentration, and urinary cyclic GMP excretion were correlated and were proportional to the degree of cardiac failure, as assessed by the increase in right ventricular mass and the decrease in blood pressure. In male SHR (aged 6-24 months), plasma ANF and urinary cyclic GMP were correlated, increased with age, and were proportional to the heart to body weight ratio. These correlations between plasma ANF, daily urinary cyclic GMP excretion, and left ventricular hypertrophy persisted in two year old SHR. The presence of pleural extravasation in these old animals was also characterised by significant increases in both plasma ANF and urinary cyclic GMP. The plasma ANF and the daily urinary cyclic GMP excretion were negative prognostic indicators of life expectancy in two year old SHR. CONCLUSIONS--Urinary cyclic GMP excretion, correlated with the plasma ANF level, is a non-invasive indicator of congestive heart failure in two models of overloaded left ventricle in rats.

Atrial natriuretic factor binding sites in experimental congestive heart failure

A quantitative in vitro autoradiographic study was performed on the aorta, renal glomeruli, and adrenal cortex of cardiomyopathic hamsters in various stages of heart failure and correlated, in some instances, with in vivo autoradiography. The results indicate virtually no correlation between the degree of congestive heart failure and the density of 125I-labeled atrial natriuretic factor [(Ser99, Tyr126)ANF] binding sites (Bmax) in the tissues examined. Whereas the Bmax was increased in the thoracic aorta in moderate and severe heart failure, there were no significant changes in the zona glomerulosa. The renal glomeruli Bmax was lower in mild and moderate heart failure compared with control and severe heart failure. The proportion of ANF B- and C-receptors was also evaluated in sections of the aorta, adrenal, and kidney of control and cardiomyopathic hamsters with severe heart failure. (Arg102, Cys121)ANF [des-(Gln113, Ser114, Gly115, Leu116, Gly117) NH2] (C-ANF) at 10(-6) M displaced approximately 505 of (Ser99, Tyr126)125I-ANF bound in the aorta and renal glomeruli and approximately 20% in the adrenal zona glomerulosa in both series of animals. These results suggest that ANF may exert a buffering effect on the vasoconstriction of heart failure and to a certain extent may inhibit aldosterone secretion. The impairment of renal sodium excretion does not appear to be related to glomerular ANF binding sites at any stage of the disease.

Radiographic pulmonary congestion in end-stage congestive heart failure

Chest radiography is considered an accurate technique for evaluating the presence and degree of congestive heart failure 1 (CHF). Radiographic evidence of redistribution of pulmonary blood flow and interstitial and alveolar edema is an established indicator of pulmonary artery wedge pressure in both acute and chronic forms of CHF. 2 It is believed that the absence of these radiographic findings is inconsistent with severe CHF and, specifically, elevations of pulmonary artery wedge pressure. 3–5 Much work describing the utility of chest radiography in the diagnosis and management of patients with CHF was carried out before the advent of potent diuretics and vasodilator agents. 6 Currently, many treated patients with end-stage CHF do not have clinical congestion and may die suddenly despite apparent hemodynamic compensation. 7,8 This report examines the chest radiographic abnormalities observed in patients with chronic severe CHF and marked elevation of pulmonary artery wedge pressure.

Prognosis and long-term results of surgically treated aortic stenosis.

A total of 675 patients (mean age 60 +/- 11 years, range 22-85, 71% males) with calcified pure aortic stenosis (490) or mixed lesions (185) had an aortic prosthesis: 290 Starr-Edwards, 147 Bjork, 18 other mechanical valves, 163 pericardial xenografts, 57 porcine xenografts; 76 patients simultaneously underwent a coronary bypass, 12 a replacement of ascending aorta, and six a mitral valvuloplasty. Preoperatively, 67% were in functional class III or IV (NYHA); 69.5% had a coronary arteriography: significant coronary stenosis was observed in 27% of patients. The operative mortality was 6.8% depending on the functional class at surgery, age (4.9% before 70 years, vs. 12.5% after), and the date of surgery (8.1% before 1983 vs. 3.7% after). The 10- and 15-year actuarial survival rates were 62 +/- 3% and 44 +/- 4%, respectively. No significant differences were observed between patients with pure aortic stenosis and mixed aortic lesions. In patients over 70 years, the survival rates were 71 +/- 5% at five years and 51 +/- 10% at 10 years. Age, functional class, degree of congestive heart failure, and degree of cardiomegaly were the main preoperative predictors of late death. At 10 years, 88% of patients were free from myocardial dysfunction, 87% from thromboembolic events, and 89% from haemorrhages. We conclude that in this type of valvulopathy, short- and long-term surgical results are good despite the fact that most patients are elderly and in an advanced functional class.

Hyponatraemia as a marker for high renin heart failure.

The factors that might activate the renin-angiotensin system in treated heart failure were explored. Serum Na+ correlated inversely with plasma renin activity. The degree of congestive heart failure measured by right atrial pressure, pulmonary capillary wedge pressure, cardiac index, and systemic vascular resistance did not correlate with plasma renin activity. Similarly, renal function as measured by blood urea nitrogen, creatinine, and urinary Na+ excretion did not correlate with plasma renin activity. In a prospectively screened group, seven patients with congestive heart failure who were found to be hyponatraemic had plasma renin activities greater than 15 ng/ml per h. Serial determinations in one patient showed plasma renin activity to vary inversely with the serum Na+. It is concluded that serum sodium can be used to identify those patients with congestive heart failure who have a high plasma renin activity. The value of identifying these high renin heart failure patients was seen in their response in four cases to specific therapy with a converting enzyme inhibitor.

Influence of age on theophylline clearance in patients with chronic obstructive pulmonary disease.

Theophylline total body clearance was calculated in 59 adult patients requiring intravenous aminophylline therapy. Group 1 consisted of 36 chronic obstructive pulmonary disease patients who were cigarette smokers without other conditions known to alter theophylline kinetics (age range: 22 to 79 years). Group 2 consisted of 23 chronic obstructive pulmonary disease patients who were cigarette smokers with a similar degree of congestive heart failure, but free of other characteristics or diseases that affect theophylline disposition (age range: 41 to 81 years). When individual theophylline total body clearance values were plotted against age in each group, poor correlation coefficients were found, indicating that age is not a good predictor of total body clearance of theophylline (group 1: r = 0.101; group 2: r = 0.276). Each group was also broken into 'younger' and 'older' patients. No significant differences in theophylline total body clearance values were found between the younger and older patients for either group I or 2, suggesting that a theophylline dosage reduction is not necessary in cigarette smoking patients over an arbitrary age limit.

Safety and efficacy of procainamide infusions

Thirty-four patients who were resistant to conventional doses of lidocaine received procainamide intravenously according to a pharmacokinetically designed two infusion technique. A mean peak serum concentration of 7.1 mg/liter was achieved with an average loading dose of 989 mg administered over 1 hour. A mean steady state serum concentration of procainamide of 6.5 mg/liter was achieved with a mean dose of 64.4 mg/kg body weight for the first 24 hours of treatment. Dose, renal impairment, the degree of congestive heart failure and acetylator status influenced the steady state serum concentration of procainamide. Dangerous ventricular arrhythmias were abolished in 74 percent of the patients at a steady state level of 6.9 ± 3.7 mg/liter (mean ± standard deviation). Nonresponders to procainamide had a mean steady state serum concentration of procainamide of 4.2 ± 2.1 mg/liter (P < 0.05). Systolic and diastolic blood pressures decreased moderately (10 and 8 percent, respectively), and heart rate decreased 11 percent. The infusion was interrupted in one patient because of hypotension. The duration of electrocardiographic conduction intervals was increased slightly in some patients. It is concluded that procainamide administered by this two infusion method is effective and well tolerated by most patients.

Immunological results in myocardial diseases.

Immunological studies have shown new diagnostically important changes in alcoholic and viral myocarditis, as well as in congestive cardiomyopathy. Increased heart size correlated with the degree of congestive heart failure, as well as with negative immunofluorescence and an increased IgA concentration in the serum. These findings may serve as a diagnostic aid in patients with myocardial disease due to alcohol abuse. Viral heart disease is characterized by a variety of symptoms and nuclear antibodies (IgM) can be of help in the differential diagnosis. Heart muscle tissue of patients with congestive cardiomyopathy preferentially binds IgG and IgA. In addition to the other changes these findings are of diagnostic importance. It seems likely that results similar to those obtained for humoral antibodies in congestive cardiomyopathy will apply in the correlation of the haemodynamic status of the patients. The pathophysiological implication of these findings is not clear at present, but the evolution of congestive cardiomyopathy appears to be associated with binding of immunoglobulin to the myocardium, as well as with humoral antiheart antibodies.