Are the elderly different? Factors influencing mortality after percutaneous coronary intervention with stent implantation.

BACKGROUND: The aim of this study was to investigate factors influencing mortality after percutaneous coronary intervention (PCI) in patients aged ≥ 75 years compared to younger patients. PATIENTS AND METHODS: A total of 1,809 coronary heart disease (CHD) patients after PCI with stent implantation in our hospital were assessed. Kaplan-Meier analyses with log-rank test and Cox regression analyses were performed on three predefined models concerning primary endpoint of all-cause mortality. Model 1 was a univariate analysis of the influence of age dichotomized by age 75 years on the primary endpoint. Model 2 included age and classical cardiovascular risk factors (CVRFs, e.g., body mass index (BMI), smoking, diabetes, and hypertension). Model 3 consisted of age, classical CVRFs, and additional factors (e.g., medication; hemoglobin, peripheral arterial disease (PAD), low-density lipoprotein cholesterol (LDL-C) and creatinine levels, and left ventricular ejection fraction (LVEF)). RESULTS: In the mean follow-up of 137 ± 61 weeks 375 patients died. Age ≥ 75 years was significantly related to mortality in all models. In model 3, previous stroke, PAD, diabetes, elevated levels of serum creatinine, and increased LDL-C were related to elevated mortality, higher hemoglobin levels, and LVEF > 50% were associated with decreased mortality in all patients and in patients < 75 years. In patients ≥ 75 years arterial hypertension was associated with poor outcome (hazard ratio (HR) 7.989, p = 0.040), previous antiplatelet therapy showed reduced mortality (HR 0.098, p = 0.039). CONCLUSION: Although risk factors such as previous stroke, PAD, diabetes, renal insufficiency, and anemia were predictors for death in all patients and patients < 75 years, in the elderly only arterial hypertension increased, whereas treatment with platelet inhibitors decreased mortality.

[Cardiac biomarkers in perioperative medicine : significance for noncardiac surgery patients]. / Kardiale Biomarker in der perioperativen Medizin : Stellenwert bei nichtherzchirurgischen Patienten.

Perioperative detection of cardiac biomarkers may help to identify patients at risk. Whether detection of these markers will be recommended in the preoperative setting for patients with cardiac diseases in the future has to be discussed as large prospective trials on this topic are missing. For preoperative evaluation of cardiac insufficiency quantification of brain natriuretic peptide (BNP) and amino-terminal pro-brain natriuretic peptide (NT-proBNP) are useful markers. Troponin is the marker of choice for detection of myocardial ischemia/infarction in the postoperative setting. In unstable patients coronary angiography and/or percutaneous coronary intervention (PCI) are indicated. However, in stable patients the decision for coronary angiography and/or PCI has to be made in each patient individually after interdisciplinary discussion between anesthesiologists, cardiologists and surgeons.

Impaired ventilatory efficiency in chronic heart failure: possible role of pulmonary vasoconstriction.

BACKGROUND: Patients with chronic heart failure show impairment of ventilatory efficiency, defined as the relation between ventilation and carbon dioxide output. It is caused by ventilation of excess physiologic dead space. We hypothesized a role of active vasoconstriction in the increase of physiologic dead space, presumed to lead to alveolar hypoperfusion. METHODS AND RESULTS: In 57 patients with chronic heart failure (New York Heart Association classification II through IV, ejection fraction 25.6%+/-10.4%) and 7 control subjects, gas exchange at rest and on exercise was compared with hemodynamic measurements and, in a subgroup of 15 patients, with endothelin-1, epinephrine, and norepinephrine levels in the pulmonary and systemic circulation. Ventilatory efficiency at rest (VE/VCO2 ratio) correlated with ventilatory efficiency on exercise (VE vs VCO2 slope). Impairment of ventilatory efficiency correlated strongly negative with exercise tolerance (maximal oxygen uptake: r = -0.67) and cardiac output (r = -0.66) and positive with pulmonary hypertension (mean pulmonary artery pressure: r = 0.69, pulmonary vascular resistance: r = 0.60). None of the vasoconstrictors correlated with reduction of ventilatory efficiency in the subgroup studied. CONCLUSIONS: Impairment of ventilatory efficiency in chronic heart failure is correlated with resting pulmonary artery pressures and associated with the impairment of exercise capacity. An imbalance of pulmonary vascular tone probably leads to both pulmonary hypertension and alveolar hypoperfusion.

Systemic inflammation in patients with heart failure.

AIMS: We hypothesized that chronic heart failure as a model of systemic hypoxia may result in systemic inflammation. The signs of a systemic inflammatory response should disappear after successful mechanical circulatory support using biventricular assist device systems. METHODS AND RESULTS: Plasma levels of cytokines (IL-6, IL-8, TNF-alpha) and soluble adhesion molecules (sVCAM, sE-, sL-, sP-Selectin) were determined in samples obtained from patients with chronic heart failure NYHA classes II-III, patients with overt cardiogenic shock before and after implantation of a mechanical assist-device system ('Berlin Heart') and in patients with coronary artery disease as a control. Elevated levels of cytokines and soluble adhesion molecules could be observed in patients with cardiogenic shock, although slightly decreased levels of soluble adhesion molecules were also detectable in patients with chronic heart failure NYHA classes II-III. The signs of systemic inflammation disappeared following successful mechanical circulatory support, but persisted in patients who developed infectious complications. CONCLUSIONS: Our data suggest that a systemic hypoxic and inflammatory syndrome is manifested during end-stage heart failure, such as in patients with sepsis or who have suffered non-infectious insults. During mechanical circulatory support, elevated levels of inflammatory mediators may be indicative of persistent peripheral hypoxia associated with a high risk for infection or sepsis. Therefore, the monitoring of inflammatory mediators should be evaluated as markers of the effectiveness of this therapy.

Ventilatory efficiency and exercise tolerance in 101 healthy volunteers.

The ventilatory equivalent for CO2 defines ventilatory efficiency largely independent of metabolism. An impairment of ventilatory efficiency may be caused by an increase in either anatomical or physiological dead space, the latter being the most important mechanism in the hyperpnoea of heart failure, pulmonary embolism, pulmonary hypertension and the former in restrictive lung disease. However, normal values for ventilatory efficiency have not yet been established. We investigated 101 (56 men) healthy volunteers, aged 16-75 years, measuring ventilation and gas exchange at rest (n = 64) and on exercise (modified Naughton protocol, n = 101). Age and sex dependent normal values for ventilatory efficiency at rest defined as the ratio ventilation:carbon dioxide output (VE:VCO2), exercise ventilatory efficiency during exercise, defined as the slope of the linear relationship between ventilation and carbon dioxide output (VE vs VCO2 slope), oxygen uptake at the anaerobic threshold and at maximum (VO2AT, VO2max, respectively) and breathing reserve were established. Ventilatory efficiency at rest was largely independent of age, but was smaller in the men than in the women [VE:VCO2 50.5 (SD 8.8) vs 57.6 (SD 12.6) P < 0.05]. Ventilatory efficiency during exercise declined significantly with age and was smaller in the men than in the women (men: (VE vs VCO2 slope = 0.13 x age + 19.9; women: VE vs VCO2 slope = 0.12 x age + 24.4). The VO2AT and VO2max were 23 (SD 5) and 39 (SD 7) ml O2 x kg x min(-1) in the men and 18 (SD 4) and 32 (SD 7) in the women, respectively, and declined significantly with age. The VO2AT was reached at 58 (SD 9)% VO2max. Breathing reserve at the end of exercise was 41% and was independent of sex and age. It was concluded from this study that ventilatory efficiency as well as peak oxygen uptake are age and sex dependent in adults.

Angiotensin-converting enzyme inhibitors in preventing remodeling and development of heart failure after acute myocardial infarction: results of the German multicenter study of the effects of captopril on cardiopulmonary exercise parameters (ECCE).

Early action of angiotensin-converting enzyme (ACE) inhibitors after myocardial infarction (MI) has been shown in large scale clinical trials to reduce mortality over the first weeks. However, the mechanisms involved are yet unclear and several trials showed a tendency toward a small, albeit unexpected, rise in cardiogenic shock or mortality. Since cardiopulmonary exercise testing (CPX) has become a "gold standard" in assessing the severity of heart failure, we studied--after finishing a pilot trial--the effect of captopril versus placebo in 208 patients who were individually titrated (titrated dose, mean 46/69 mg/day after 7 days/4 weeks, respectively) in order to preserve their blood pressure in the acute phase of myocardial infarction; we followed the development of congestive heart failure (CHF) over 4 weeks by measuring oxygen consumption. After 4 weeks, overall oxygen consumption at the anaerobic threshold (VO2-AT; 13.7 vs 13.1), maximal oxygen consumption (VO2max 19.3 vs 18.9 mL/kg per min) and exercise duration (896 vs 839 sec) showed a nonsignificant difference in favor of the captopril group. The predefined, categorized, combined endpoint of severe heart failure or death (heart failure necessitating ACE inhibition, VO2max < 10 mL/kg per min, or death) was significantly reduced in the captopril group (n = 7/104) versus placebo (n = 18/104; p = 0.03). Differences were mainly caused by fewer CHF events (delta n = 10). We conclude that ACE inhibition with individualized dose titration markedly reduces the 4-week incidence of severe heart failure or death; > 10 patients per 100 treated gained major benefits from this therapy.

Respiratory muscle weakness and normal ventilatory drive in dilative cardiomyopathy.

BACKGROUND: In dilative cardiomyopathy several factors influence dyspnoea. Patients with chronic heart failure may demonstrate impairment of breathing pattern, ventilatory drive and respiratory muscle strength, as well as reduction of ventilatory efficiency. The purpose of this study was to evaluate whether dilative cardiomyopathy is accompanied by changes in breathing pattern, respiratory muscle weakness and ventilatory neural drive. METHODS: We investigated 47 patients (36 men, mean age = 47.8 +/- 11.2 years) with chronic heart failure due to dilative cardiomyopathy, and 30 healthy subjects (10 men, mean age = 35.4 +/- 11.7 years) served as controls. Patients and controls underwent evaluation of left ventricular ejection fraction by 2D echocardiography, spirometry, body plethysmography, mouth occlusion pressure and respiratory muscle strength, as well as by submaximal treadmill exercise testing with gas exchange measurements. The patients' results were compared to controls and predicted standard normal values, and evaluated for differences according to the degree of severity of functional impairment. RESULTS: Patients with dilative cardiomyopathy demonstrated a slight reduction in lung volumes (15% of the patients with obstructive and 15% with restrictive lung function pattern) and diffusion capacity (20.4 +/- 6.8 vs 15.4 +/- 6.7 ml.min-1.kPa-1; P < 0.01). In neural drive, as assessed by mouth occlusion pressure, there was no significant difference between patients and controls. There was a slight but significant reduction in respiratory muscle strength, as assessed by measuring maximal inspiratory pressure in patients with dilative cardiomyopathy (6.7 +/- 2.4 kPa vs 8.6 +/- 3.5 kPa; P < 0.01). The observed changes were more pronounced in the severe chronic heart failure patients (with a reduction in ventilatory efficiency) whereas no relationship among indices of cardiac or respiratory function was found. CONCLUSIONS: Patients with chronic heart failure due to dilative cardiomyopathy develop respiratory muscle weakness without changes in neural ventilatory drive, and slight changes in breathing pattern related to the severity of the disease.

Acetylcholine causes dose dependent increase in pulmonary flow in patients with chronic heart failure and elevated pulmonary vascular resistance.

Elevated pulmonary vascular resistances occur to a variable degree in patients with chronic congestive heart failure (CHF). These might be caused by increased levels of endogenous vasoconstrictors, defective endothelial vasodilatory mechanisms or structural vascular abnormalities. To determine the contribution of defective endothelial mediated vasodilation, we tested 10 patients with CHF due to coronary artery disease (n = 4) or dilated cardiomyopathy (n = 5), and congenital corrected transposition of the great arteries (n = 1) (median pulmonary artery pressure 36 mmHg, range of pulmonary vascular resistance 0.94-10.7 WE). Patients were in median functional class NYHA III, median left ventricular ejection fraction was 21%, median oxygen uptake at the anaerobic threshhold was 8.25 ml/kg/min. Flow was measured by a flow wire (0.018 inch) positioned in a pulmonary artery branch with a diameter of 3-8 mm determined by intravascular ultrasound before. Acetylcholine infusion was adjusted to 10(-6), 10(-5) and 10(-4) molar concentrations in the pulmonary artery branch. A dose dependent increase in flow between 64 to 140% was seen in 8 out of 10 patients. We conclude: Acetylcholine mediated vasodilation is found in patients with CHF and elevated pulmonary vascular resistances.

Exertional hyperpnea in patients with chronic heart failure is a reversible cause of exercise intolerance.

BACKGROUND: Hyperpnea in chronic heart failure occurs even in the absence of considerable impairment of lung function. It is caused by altered respiratory pattern with rapid shallow breathing and ventilation-perfusion mismatch, so far thought to be irreversible. OBJECTIVES: To test the underlying pathophysiologic disorders and the reversibility of this hyperpnea, i.e., the increased ventilatory response to exercise and its impact on exercise tolerance, 17 patients with chronic heart failure were evaluated before and 4 weeks after adjustment of heart failure therapy with diuretics and ACE inhibitors, and results were compared with normal volunteers. METHODS: Ventilatory response to exercise was measured during treadmill exercise by calculation of the slope of the linear relation between minute ventilation (VE) and carbon dioxide output (VCO2) and compared to NYHA class, oxygen consumption at the gas exchange anaerobic threshold (VO2 AT), maximal oxygen uptake (VO2 max) and ventilation of physiological dead space. RESULTS: VE vs VCO2 slope was related to severity of heart failure (NYHA class). Elevation of VE vs VCO2 slope was strongly correlated to elevated ventilation of physiologic dead space. Patients were divided into responders (significant decrease of VE vs VCO2 slope of at least 5 l/l I CO2) and nonresponders (decrease of VE vs VCO2 slope less than 5 I or increase). Responders revealed an increase of VO2 AT (7.4 +/- 2.6 to 11.7 +/- 2.1 ml O2/kg/min; p = 0.01) and VO2 max (11.2 +/- 2.8 to 17.4 +/- 5.3; p = 0.005), while nonresponders showed a non significant decrease of oxygen consumption (VO2 AT 9.6 +/- 3.7 to 9.0 +/- 3.7; peak VO2 14.6 +/- 6.1 to 14.4 +/- 6.4), despite adjusted heart failure therapy. CONCLUSION: Exercise hyperpnea in heart failure is mainly caused by ventilation of excess physiologic dead space and strongly contributes to severity of symptoms. Ventilatory response to exercise can be improved by adjustment of heart failure therapy in a considerable proportion of patients. Improvement is associated with an increase in aerobic capacity. Ventilation-perfusion mismatch is a major and modifiable factor determining exercise tolerance in patients with chronic heart failure.

[Percutaneous "high risk" angioplasty with prophylactic cardiopulmonary support. High risk PTCA with mechanical circulatory support]. / Die perkutane "Hochrisiko" -Angioplastie unter prophylaktischem Kardiopulmonalen Support. Hochrisiko PTCA mit mechanischer Kreislaufassistenz.

With improved technology and development of several mechanical assist devices, the indications of percutaneous transluminal coronary revascularization have been extended. In 39 patients (30 men, mean age = 60.1 +/- 8.1 years) with angina pectoris or heart failure, with poor operative risk-benefit ratio and ejection fraction < 35% and/or target vessel supplying > 50% of the viable myocardium, we performed assisted percutaneous transluminal coronary revascularization. Intraortic balloon counterpulsation (n = 16), extracorporal circulation (n = 21), or hemopump (n = 2) were used for mechanical support. Complete 6-week follow up was possible in 27 patients. An improvement of left-ventricular function (patients with EF < or = 35% demonstrated an improvement: 27 +/- 7 vs 36 +/- 10%, p < 0.05), heart failure (patients with EF < or = 35% demonstrated an improvement of maximal oxygen uptake: 14 +/- 4 vs 17 +/- 4 ml/kg/min; p < 0.05) and a marked improvement of angina (23/38 demonstrated CCS-improvement of at least one class) was found. Hospital mortality was as low as 2.6%. Major postinterventional complications included nonfatal myocardial infarction (n = 2), fatal retroperitoneal bleeding (n = 1), pulmonary edema (n = 1), nonfatal ventricular fibrillation (n = 1), cerebrovascular event without residual (n = 1), and deep vein thrombosis (n = 4). In conclusion, assisted percutaneous revascularization was successful in a high risk subset of patients with increased surgical risk and/or poor ventricular function.

Experiences with ACE inhibitors early after acute myocardial infarction. Rationale and design of the German Multicenter Study on the Effects of Captopril on Cardiopulmonary Exercise parameters post myocardial infarction (ECCE).

Left ventricular damage by necrosis of myocardial tissue can lead to compromise of left ventricular function, to left ventricular volume increase and ultimately to development of heart failure. This sequence in the pathophysiology has been shown to be blunted by ACE inhibitors. Volume increase, however, can also be helpful in restoring stroke volume and ameliorate elevation of filling pressures. Furthermore, very early institution of ACE inhibition has failed to improve short-term mortality after myocardial infarction in one large trial. The aim of the ECCE trial therefore is, to investigate the early effects of the ACE inhibitor captopril on compromise of exercise capacity, thought to be a first measurable sign of developing heart failure. The ECCE trial is a randomized, seven-center investigation, studying the effects of ACE inhibition on oxygen uptake in a double blind, placebo controlled design in a group of 204 patients. Sample size was calculated on the basis of a pilot trial. The study design and first not unblinded data of 104 patients are presented. The population consists of predominantly male patients with mostly first myocardial infarction. They were admitted to hospital within five hours of onset of chest pain. End-diastolic volumes were normal, but ejection fraction was moderately compromised. ACE inhibition was started after the first day, but within 72 hours of onset of chest pain. After four and after twelve weeks, oxygen uptake was considerably below expected values and one third of the patients had severe compromise of exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

[Abscessing pneumonia]. / Az abscedáló pneumoniákról.

Among the patient of a prospective study aimed to recognize the epidemiological and clinical characteristics of pneumonias, cavitating pneumonia occurred in 12.5%, typical lung abscess in 24 cases and necrotizing pneumonia in 11 cases. The illness was secondary in 4 cases. Predisposing factors were present in the majority of the patients. Assumable pathogen was detected with microbiological examinations in 24 cases. 20 patient recovered--19 by antibiotic therapy and one by surgery--were operated on the average in 7 weeks. Complication occurred in 15 patients 7 of them died. The prognosis of cavitating pneumonias is favourable, however the mortality is high in the secondary cases.