Sleep apnoea in ischaemic heart disease: differences between acute and chronic coronary syndromes.

OBJECTIVE: To evaluate the incidence of sleep apnoea in acute and chronic coronary syndromes. DESIGN: Analysis of sleep and breathing characteristics in a polysomnographic study. SETTING: Cardiology department in tertiary referral centre. PATIENTS: 23 patients were studied soon after acute myocardial infarction (group 1), 22 after clinical stabilisation of unstable angina (group 2), and 22 who had stable angina (group 3). Conditions liable to cause sleep apnoea, such as obesity, chronic obstructive pulmonary disease, neurological disorders, or the use of benzodiazepines, were exclusion criteria. MAIN OUTCOME MEASURES: Sleep apnoea and hypopnoea, oxygen saturation, and sleep indices evaluated soon after clinical stabilisation in groups 1 and 2 and also in group 3. RESULTS: Sleep apnoea, mainly of the central type, was equally present in groups 1 and 2 (mean (SD) apnoea-hypopnoea index: 11.10 (19.42) and 14.79 (20.52), respectively) and more severe than in group 3 (2.82 (6.43), p < 0. 01). Total time spent at SaO(2) < 90%, although significantly greater in group 1 and 2 (0.89 (2.4), 1.42 (3.23) min) than in group 3 (0.01 (0.05) min, p < 0.05), was clinically irrelevant. More arousals per hour of sleep (p < 0.05) were detected in group 1 (5.15 (3.71)) and group 2 (5.31 (2.14)) than in group 3 (2.83 (1.51)). CONCLUSIONS: Sleep apnoea, chiefly of the central type, not only characterises acute myocardial infarction, as found by others, but also unstable angina studied after recent stabilisation. Patient selection by exclusion of other causes of breathing disorders shows that coronary disease related apnoea is absent in the chronic coronary syndrome. In acute syndromes the lack of clinically significant apnoea related oxygen desaturation, together with the low associated incidence of major ischaemic and arrhythmic events, suggests that sleep apnoea is benign in these circumstances, despite a worsening of sleep quality.

Medium-term effectiveness of L-thyroxine treatment in idiopathic dilated cardiomyopathy.

BACKGROUND: In dilated cardiomyopathy, short-term administration of L-thyroxine (100 micrograms/ day) improves cardiac and exercise performance without changing the heart's adrenergic sensitivity. The aim of this study was to test the medium-term (3 months) efficacy of L-thyroxine (10 patients) compared with placebo (10 patients) and to find out whether later effects are obtainable. METHODS: Echocardiographic parameters in the control state and during acute changes of left ventricular afterload, cardiopulmonary exercise test, and hemodynamic parameters, including cardiac beta 1 responses to dobutamine, were obtained before and at the end of treatment. RESULTS: Significant (P < 0.05) changes were observed only with the active drug. After L-thyroxine, patients did not show evidence of chemical hyperthyroidism, despite the increase in thyroxine and the reduction in thyroid-stimulating hormone plasma levels. Cardiac performance improved, as shown by the increase in the left ventricular ejection fraction and rightward shift of the slope of the relation left ventricular ejection fraction/end-systolic stress. Resting cardiac output increased, and the left ventricular diastolic dimensions and systemic vascular resistances decreased. The responses of cardiac output and heart rate to dobutamine infusion were also enhanced. Functional capacity markedly improved, together with an increase in peak exercise cardiac output. CONCLUSION: L-thyroxine does not lose its beneficial effects on cardiac and exercise performance on medium-term administration and does not induce adverse effects. In addition to the short-term study, the left ventricular diastolic dimensions were decreased. An upregulation of beta 1 receptors might explain the cardiac response to dobutamine.

Systemic to pulmonary bronchial blood flow in heart failure.

STUDY OBJECTIVE: The aim of this study was to measure systemic to pulmonary blood flow from bronchial circulation (Qbr[s-p]) in patients with heart failure. DESIGN: In the absence of pulmonary and coronary flows, Qbr(s-p) is the volume of blood accumulating in the left side of the heart; Qbr(s-p) was measured during total cardiopulmonary bypass for coronary artery surgery; bronchial blood was vented through a cannula introduced into the left side of the heart and its volume was measured. PATIENTS: Patients were subdivided according to the presence for more than 6 months (group 1, n = 6) or less than 2 months (group 2, n = 7), or the absence of heart failure (group 2, n = 15). MEASUREMENTS AND RESULTS: Qbr(s-p) was 89 +/- 18* mL/min, 27 +/- 3, 22 +/- 2, in groups 1, 2, and 3, respectively (* = p < 0.01 group 1 vs groups 2 and 3). During total cardiopulmonary bypass, pulmonary venous pressure approximates atmospheric pressure and no differences between groups were observed in systemic artery pressure, extracorporeal circulation pump flow, and airway pressure. Therefore, vascular resistance through the bronchial vessels draining into the pulmonary circulation is reduced in patients with heart failure for more than 6 months (group 1). CONCLUSIONS: During total cardiopulmonary bypass, Qbr(s-p) is increased in patients with chronic heart failure. Since with elevated pulmonary vascular pressure blood flow through Qbr(s-p) vessels is from the pulmonary to the systemic circulation, the lower resistance observed in group 1 suggests that bronchial vessels might contribute to reduced lung fluid overload in patients with chronic heart failure.

Obstruction of the right pulmonary artery by an aortic aneurysm complicating previous coronary bypass grafting.

We report a case of right main pulmonary artery compression due to a type II dissecting aortic aneurysm simulating massive pulmonary artery embolism. Aortic tear and intimal splitting developed around an aortocoronary bypass graft performed 11 months earlier. Ultrasound detected the aortic aneurysm and pulmonary hypertension, and excluded emboli in the pulmonary artery. Pulmonary angiography explained the lung involvement, showing compression of the right main pulmonary artery. Coronary and aortic angiograms demonstrated that the aortic aneurysm developed around the right venous bypass graft. Surgery confirmed the angiographic findings and the pathogenesis of the syndrome.

Usefulness of L-thyroxine to improve cardiac and exercise performance in idiopathic dilated cardiomyopathy.

The short-term effects of L-thyroxine (100 micrograms/day, 10 patients) and placebo (10 patients) on idiopathic dilated cardiomyopathy were compared. Before and at the end of the treatment, a hemodynamic study was performed in the control state and during dobutamine infusion. A cardiopulmonary exercise test was also performed with hemodynamic monitoring. An echocardiogram was recorded in the control state and during acute changes of left ventricular afterload. Plasma levels of triiodothyronine, thyroxine, thyroid-stimulating hormone and norepinephrine were measured. Placebo was ineffective. After administration of L-thyroxine all patients had normal thyroid function. The increase in left ventricular ejection fraction and the rightward shift of the slope of left ventricular ejection fraction/end-systolic stress relation (p < 0.05) indicated an improvement in the cardiac inotropic state. This proved to be independent of adrenergic influences by the unchanged beta 1 response to dobutamine. A decrease in resting systemic vascular resistances and an increase in cardiac output (p < 0.05) were also observed. Cardiopulmonary effort parameters improved (p < 0.05) without hemodynamic changes at peak exercise. It is concluded that L-thyroxine short-term administration improves cardiac and exercise performance in patients with chronic heart failure, without modifying the adrenergic support to the heart and the circulatory parameters at peak exercise.

Control of pulmonary vasomotility in congestive heart failure.

Although enhanced sympathetic tone is a well-known component of the autonomic imbalance of heart failure, its influence on pulmonary vasomotility is undefined. We investigated the pulmonary circulation in 12 patients with congestive heart failure in NYHA functional class III and in a control group of 10 normal subjects. Sympathetic influence on pulmonary vessels was studied through adrenergic activation by the arithmetic test and the cold pressor test. A rubber balloon was distended in the inferior vena cava to reduce transpulmonary flow and its influence on vascular tone. In normal individuals the arithmetic test caused pulmonary vasodilation, probably because of the mechanical effect of a largely enhanced flow: in fact, caval obstruction unmasked a neurogenic vasoconstrictor response to the arithmetic test by simply reducing the amount of cardiac output increase. In patients with heart failure, cardiac output and pulmonary arteriolar resistance remained steady during the arithmetic test, no matter what the condition of the venous return was. The cold pressor test was always a vasoconstrictor stimulus, but only in normal subjects was vasoconstriction potentiated by reducing, with caval obstruction, transpulmonary flow and its vasodilatory influence. From these data an attenuation of the sympathetic influence on pulmonary vessels in congestive heart failure seems to be likely. This might be explained as the result of modifications of pulmonary vessels rather than of reduced sympathetic excitability since circulating catecholamine levels varied to similar extents in the two groups during the tests. In congestive heart failure interstitial edema and vascular wall imbibition might increase pulmonary vessel tone and decrease vascular receptor availability. Lower reactivity to sympathetic stimuli, particularly to the vasoconstrictor ones, would ensue.

Postoperative atelectasis reexpansion by selective insufflation through a balloon-tipped catheter.

Although treatment of refractory atelectasis has been improved by pulmonary insufflation through FOB with balloon cuff, low pulmonary compliance and high critical opening pressure of alveoli in the atelectatic areas require a more selective approach to prevent pressure dispersion to highly compliant zones. To achieve the highest insufflation selectivity and reduce patient discomfort, we have devised a small caliber balloon-tipped catheter to easily reach even the minor branches of the bronchial tree. This result was obtained by utilizing the performed curve of the catheter distal end after withdrawing the internal stylet. The catheter was introduced through the nostrils (16 patients) or through an endotracheal tube (two patients) and advanced under fluoroscopic guidance. Reexpansion of atelectatic areas was accomplished by repeated air injections through a 60-ml syringe. No complications were observed. Complete disappearance of x-ray film evidence of atelectasis was obtained in 15 patients and partial reexpansion in 3 patients.

[The improvement in physical exercise capacity in dilated cardiomyopathy during short-term treatment with L-thyroxine]. / Miglioramento della capacità di esercizio fisico nella cardiomiopatia dilatativa durante trattamento a breve termine con L-tiroxina.

Reduced left ventricular function and other factors, such as vascular resistances, redistribution of cardiac output and impaired muscular metabolism, limit exercise performance in chronic heart failure. Thyroid hormones have a positive cardiac inotropic effect, stimulate protein synthesis (particularly at muscular level) and reduce peripheral vascular resistances with consequent increase of cardiac output. Therefore, it is possible that thyroid hormones can improve exercise performance in chronic heart failure. We have administered L-thyroxin (100 mcg/die) for 1 week to 9 patients affected by primary dilated cardiomyopathy. All the patients were euthyroid (T3 = 1.06 +/- 0.1 mcg/ml, T4 = 8.5 +/- 1.9 mcg/dl, TSH = 1.32 +/- 0.7 mU/ml) and in II-III NYHA functional class. Before starting the treatment and at the end of it, we performed the cardiopulmonary exercise test and the echocardiogram. We also evaluated the resting hemodynamic parameters through catheterization and the plasmatic values of thyroid hormones and noradrenaline. At the end of the treatment all patients were euthyroid, despite a significant (p less than 0.05) increase of T4 (10.5 +/- 3.2 mcg/dl) and a decrease of TSH (1.1 +/- 0.1 mU/ml). Mean values of effort parameters changed as follows: peak oxygen consumption from 19.6 +/- 1.6 to 20.6 +/- 1.3 ml/min/kg, tolerance time from 460 +/- 61 to 481 +/- 60 s. These variations were not associated with changes in resting hemodynamic parameters and noradrenaline. Left ventricular ejection fraction, calculated by echocardiography, increased from 26 +/- 6 to 28.9 +/- 8% (p less than 0.05). We conclude that in dilated cardiomyopathy short term treatment with L-thyroxin significantly improves patient's response to cardiopulmonary exercise test.(ABSTRACT TRUNCATED AT 250 WORDS)

[Changes in pulmonary vascular reactivity to adrenergic stimuli in congestive heart failure]. / Modificazioni della reattività vascolare polmonare agli stimoli adrenergici nello scompenso cardiaco congestizio.

Heart failure is associated with increased activity of sympathetic nervous system. As to the latter's effector organs, attention has been mainly drawn by heart and systemic circulation. In this study we investigated whether and how the neurogenic vasomotility of the lesser circulation is modified. Therefore, we compared 12 patients with heart failure in III NYHA functional class, with 10 subjects, undergoing hemodynamic study for diagnostic reasons and found to be normal. The neurogenic reactivity of pulmonary vessels was assayed by means of 2 sympathetic stimuli: arithmetic test (AT) and cold pressor test (CPT), performed both with and without obstruction to right heart venous return. This was obtained by expanding a balloon in inferior vena cava, in order to rid the neurogenic component of pulmonary vasomotility of the interference of the normally prevailing mechanical component (consisting in adaptations to flow variations). AT caused pulmonary vasodilation in normal subjects, as a passive consequence of the increase of cardiac output and, therefore, of pulmonary flow. Caval obstruction, by simply restraining this increase, induced a clearly neurogenic vasoconstrictor response. On the contrary, in failing patients, a slight vasodilation, independently from the condition of venous return, was observed. This took place in spite of the constant absence of any variations of cardiac output, which both indicates the reduction of myocardial function and helps to show the diminished nervous influence on pulmonary circulation. On the other hand, CPT had a vasoconstrictor effect in both groups, though potentiated by the reduction of transpulmonary flow in normal subjects only.(ABSTRACT TRUNCATED AT 250 WORDS)

[The noninvasive estimation of right atrial pressure improves the Doppler evaluation of the pulmonary systolic pressure]. / La stima non invasiva della pressione atriale destra migliora la valutazione Doppler della pressione sistolica polmonare.

The right ventricular systolic pressure can be evaluated with the Doppler method through the right ventricular-atrial gradient (RV-RA gradient) and the right atrial pressure. The former is expressed by the transtricuspid velocity of flow, the latter is generally assumed. In 50 patients with elevated pulmonary pressure we tested whether ultrasounds may be utilized for the evaluation of the right atrial pressure, and whether the derived values contribute to improve the accuracy of the method. We estimated the right ventricular systolic pressure with method A: RV-RA gradient + 10; and method B: RV-RA gradient x 1.1 + 14, where 10 and 14 are the assumed right atrial pressure (mmHg). Through the collapsibility index of the inferior vena cava, taken as an ultrasound-derived index of right atrial pressure, we were able to identify 3 groups of patients with normal (Group 1, 14 cases), elevated (Group 2, 21 cases) and moderately elevated (Group 3, 15 cases) right atrial pressure, respectively. In them the right ventricular systolic pressures obtained with both method A and method B were compared to those derived with catheter. In Group 1 the non-invasive values were significantly closer to the invasive ones when calculated with method A; the same was true of method B in Group 2. In Group 3 the accuracy of the 2 methods was similar. We conclude that ultrasound assists in the non-invasive approximation of the right atrial pressure as well as in the choice of the appropriate formula, so that Doppler estimation of the right ventricular systolic pressure is improved.

Neural influences on the human pulmonary circulation as a defence reaction to volume depletion.

The role of the autonomic nervous system in the regulation of pulmonary vasomotility in man is unsettled and great emphasis is usually given to changes in flow as the main regulating mechanism. In order to simulate hypovolemia, which might reduce the mechanical influence of flow and disclose a neural mechanism, we decreased venous return through balloon distention in the inferior vena cava in 12 normal subjects, during right heart catheterization performed for diagnostic purposes. Caval obstruction was graduated to reduce cardiac output, right atrial and pulmonary arterial pressures, without altering systemic arterial pressure and heart rate. The sympathetic nervous system was activated by arithmetic and cold pressor tests. During the former, the increase in cardiac output was more than halved by venous return restraint, as compared to the unrestrained condition, and clear pulmonary vasoconstriction, instead of vasodilatation, was observed. During the cold test, cardiac output remained almost steady, in the absence as in the presence of balloon expansion. In both conditions pulmonary arteriolar resistance rose, but in the latter this increase was more than doubled. This study suggests that the autonomic nervous system is involved in the regulation of pulmonary vasomotility in man, its role being unveiled when the mechanical influence of flow is reduced by mimicking a hypovolemic state.

Pulmonary vasoconstrictor overreactivity in borderline systemic hypertension.

Raised vascular pressure and resistance and vasoconstrictor overreactivity to adrenergic stimulation are hallmarks of the pulmonary circulation in sustained primary hypertension. The aim of this study was to investigate the reasons for these disorders. In 10 males with borderline systemic hypertension, pulmonary haemodynamic variables were similar to those of an age matched group of eight normotensive subjects. In normotension, arithmetic and cold pressor tests (sympathetic activators) caused slight vasodilatation and vasoconstriction, respectively. In hypertension both tests showed an obvious vasoconstrictor effect. Restriction of blood flow through the lungs by distension of a balloon in the inferior vena cava is known to increase pulmonary vasoconstrictor reactivity in normal man. As a result of this manoeuvre, pulmonary pressure fell in the normotensive controls without variation in pulmonary vascular resistance, whereas in the hypertensive group there was an increase in resistance and the pressure did not change. In normotensive subjects with caval balloon, the sympathetic activating stimuli both became constrictor and caused vascular resistance to rise to the levels attained in the hypertensive patients during adrenergic stimulation in the absence of obstruction to venous return. In the hypertensives, these stimuli were not able to enhance the pulmonary vascular resistance further. This shows that in these patients maximal vasoconstriction was already achieved through the simple restraint of blood flow with vena caval obstruction. We suggest that in the early phases of systemic hypertension lung vessels are hypercontractile so that they overreact to hypoperfusion or to sympathetic stimulation, even before there is a stable rise in pressure and resistance.