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Combined effects of nitrates on the coronary and peripheral circulation in exercise-induced ischemia.

We compared the effects of isosorbide dinitrate (ISDN) administered by intracoronary and intravenous routes in 10 patients with severe coronary artery disease, stable effort angina, and very low exercise tolerance. Supine bicycle ergometer exercise was performed under four conditions: 1) control, 2) after intracoronary administration of 0.4 mg ISDN, 3) 1 hour later (control 2), and 4) after administration of intravenous 4 mg ISDN. At rest, intracoronary ISDN caused no significant hemodynamic effects, whereas intravenous infusion of ISDN resulted in a decline in left ventricular (LV) systolic pressure (-20 +/- 5 mm Hg), LV end-diastolic volume (-27 +/- 3%), and LV end-systolic volume (-30 +/- 4%). After intracoronary infusion of ISDN, ST segment depression and the increase in LV end-diastolic pressure and LV end-systolic volume induced by exercise were significantly less abnormal than during control (0.20 +/- 0.09 vs. 0.14 +/- 0.08 mV, 36 +/- 7 vs. 24 +/- 8 mm Hg, and 91 +/- 40% vs. 40 +/- 29%, respectively). When exercise was performed after intravenous infusion of ISDN, the above-mentioned parameters were significantly improved even further: ST segment depression to 0.05 +/- 0.07 mV, end-diastolic pressure to 14 +/- 7 mm Hg, and LV end-systolic volume to 5 +/- 11% (all p less than 0.01 compared with intracoronary ISDN). Thus, in patients with severe coronary artery disease, it is suggested that intracoronary nitrates increase coronary blood supply during effort-induced ischemia, based on significant improvements in the indirect measures of ST segment depression, LV end-diastolic pressure, and LV volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

Cardiovascular evaluation after withdrawal from chronic alcohol or cocaine-alcohol abuse.

Alcohol ingestion commonly accompanies cocaine abuse, but the effects of chronic cocaine-alcohol abuse on the circulation are undefined. Therefore, to test for evidence of cocaine-alcohol cardiac dysfunction and interference with cardiovascular nervous system reflexes, 10 normal volunteers (group I), 8 asymptomatic alcoholic patients (group II), and 15 age matched, asymptomatic cocaine and alcohol abusers (group III) underwent screening two-dimensional echocardiography, electrocardiography, a series of autonomic nervous system tests, and upright bicycle exercises. Echocardiographic indices did not differ among groups. R wave voltage was increased in group III, probably primarily due to a smaller body surface area. Heart rate (HR) and/or systolic blood pressure (SBP) responses to 60 degree tilt and to hyperventilation differed in group III (decreased HR response, while SBP increased inappropriately). Despite excellent exercise tolerance, HR response to exercise in group III (compared to group I) was decreased. These results suggest impairment of certain autonomic nervous system reflexes and, possibly, sinus node dysfunction from cocaine-alcohol abuse.

Adult↗

Exercise performance and functional impairment in asbestos-exposed workers.

Eighty-eight shipyard workers with extensive asbestos exposure were evaluated in terms of dyspnea, smoking history, x-ray film abnormalities, static pulmonary function, and exercise performance. Pulmonary function abnormalities and roentgenographic pleuropulmonary disease were more frequent in smokers. Significant dyspnea was present in 41 percent of the workers and did not correlate with smoking history, pulmonary function, or exercise performance. Despite this high frequency of dyspnea, 70 percent of all workers had normal exercise tolerance by history of exercise testing. Of the 26 workers with exercise impairment, only nine had pulmonary mechanical or gas exchange limitation. Two of these workers had asbestosis, while the other had airways obstruction without asbestosis. The prevalence of both asbestosis and asbestos-related exercise impairment in this population was 2.3 percent.

Aged↗

The role of risk stratification in the early management of a myocardial infarction.

OBJECTIVE: To review the literature on early management of myocardial infarction. DATA SOURCES: Papers published or referenced in major English-language cardiology journals for the last 15 years. STUDY SELECTION: Large recent multicenter studies and the guidelines for early management of patients with acute myocardial infarction (American College of Cardiology/American Heart Association Task Force) were emphasized. DATA SYNTHESIS: A strategy for risk stratification was developed from information available in the emergency department, from the first days of the hospitalization, and before discharge to identify patients in whom intervention might improve prognosis. CONCLUSIONS: Treatment of myocardial infarction requires establishing patency of the infarct-related artery, usually with thrombolysis. Risk stratification begins in the emergency department (phase 1) using clinical (primarily the electrocardiogram) and historical data to identify patients at risk for massive infarction. For patients at highest risk, the efficacy of thrombolytic therapy must be assured and, if not effective, emergency angiography and mechanical reperfusion should be considered. During days 2 to 5, (phase 2), patients with large amounts of ischemic myocardium, postinfarction angina, "flash" pulmonary edema, or anterior non-Q infarctions are identified and studied. Predischarge (phase 3) stratification identifies those patients at risk for early death. A previous infarction, an ejection fraction less than 0.40, pulmonary congestion during the hospitalization, delayed afterpotentials on signal-averaged electrocardiography, symptomatic ventricular ectopic beats, decreased heart rate variability, limited exercise tolerance, or ischemia on exercise testing identifies patients at high risk. Patients with jeopardized myocardium must be identified for revascularization to try to improve survival. More data are needed to determine whether angioplasty or bypass surgery will improve prognosis in these patients.

Algorithms↗

Pulmonary arteriovenous malformation as a cause of severe exertional dyspnoea.

A 48-year-old woman presented to the respiratory clinic with progressive exertional dyspnoea and an abnormal chest radiograph. Examination revealed mucosal telangiectasia and pulmonary angiography confirmed the presence of two pulmonary arterial venous malformations (PAVM). After therapeutic coil embolisation, dyspnoea was markedly improved, and exercise tolerance increased. Comparison of exercise test responses before and after this therapeutic intervention provides new insights into the physiological mechanisms of exertional dyspnoea in this condition.

Arteriovenous Malformations↗

[Evaluation of clinical effectiveness and adverse effects of Polnitrin].

In a double-blind, randomized, placebo cross-controlled trial the effectiveness and the adverse effects of two types of buccal tablets containing 5 mg nitroglycerin: Polnitrin produced by Warsaw Pharmaceutical Works POLFA and its analogue of foreign origin, were assessed. The third compared preparation was sublingual nitroglycerin in 0.5 mg tablets. The longest dissolution in the buccal cavity showed Polnitrin (mean 6.6 hours). Polnitrin significantly increased the resting heart rate during 3 hours, and during 6 hours at maximal effort. The foreign analogue decreased significantly the systolic pressure during 3 hours after application. No significant differences were noted in the effects on the basic haemodynamic parameters between the compared buccal tablets. Exercise tolerance and coronary reserve were assessed with repeated exercise tests on moving track (Marquette Case-12). Immediately after being stuck to the gum Polnitrin, its analogue and sublingual nitroglycerin significantly prolonged the marching time: total, till pain, and till ischaemia. After 6 hours the marching time till pain appearance was significantly longer after Polnitrin than after placebo or its analogue. Local adverse effects connected with the presence of the tablet in the oral vestibule may hamper the treatment with Polnitrin in some cases. The most frequent side effect were headaches which are known to occur usually after all nitrates.

Administration, Buccal↗

Exercise and heart failure.

This report will review the abnormalities of the peripheral circulation and skeletal muscle which are part of the heart failure syndrome and can limit exercise tolerance; introduce trials that have shown benefits of exercise training in a variety of heart failure patients; suggest strategies for recommending activity training in patients with heart failure. Finally, this report will identify areas where data are missing and where trials are currently being undertaken.

Exercise Therapy↗

Plasma level of atrial natriuretic peptide as an indicator of increased cardiac load in uremic patients.

Plasma levels of atrial natriuretic peptide (ANP) were measured by radioimmunoassay in 43 non-dialyzed uremic patients at rest and during maximal exercise to assess the possible relationship between plasma ANP levels and cardiac function, as judged by M-mode echocardiography and exercise tolerance. Patients with poor exercise capacity (exercise time less than 6 min) on dynamic exercise test had decreased left ventricular ejection fraction, increased left atrial diameter, and increased left ventricular mass index (LVMI), compared with patients with better exercise capacity (exercise time greater than 6 min). Plasma ANP was significantly higher in patients with poor exercise capacity and impaired cardiac function (202 pg/ml [95% confidence interval 119 to 284] at rest and 227 pg/ml [149 to 304] during exercise), compared with patients with better exercise capacity (75 pg/ml [50 to 102], p less than 0.005, and 123 pg/ml [80 to 167], p less than 0.05, respectively). Plasma ANP increased significantly (p less than 0.005) during exercise only in patients with better cardiac function. The best correlation among the variables studied was found between LVMI and plasma ANP concentration at rest (r = 0.56, p less than 0.001) and during exercise (r = 0.51, p less than 0.005), whereas neither blood pressure nor renal function showed any significant correlation with ANP levels. We conclude that plasma ANP levels are elevated in uremic patients with impaired cardiac function, correlating with increased LVMI. Plasma ANP determinations are useful in identifying increased cardiac load and consequent cardiac hypertrophy and dysfunction with known associations with increased cardiovascular mortality in patients with chronic renal failure.

Adult↗

Radiofrequency catheter modification of sinus node for inappropriate sinus tachycardia: a case report.

We present here, the case of a 22-year-old male suffering from persistent tachycardia for the past 3 years. His resting pulse rate was rarely below 100 beats/min, and it frequently increased to as high as 150 beats/min even after a minimal of activity. Associated symptoms included palpitation, chest tightness, dyspnea and presyncope, either during rest or with exercise. Propranolol and verapamil could not control the tachycardia. The application of radiofrequency energy to an area in the superior right atrium that demonstrated a discrete electrogram with earliest endocardial activation during tachycardia resulted in a decrease in sinus rate from 120 beats/min to 70 beats/min. Follow-up on Holter monitor, performed one month later, demonstrated an average heart rate of 84 beats/min (range 60-125). In exercise tolerance test, the patient exercised for 9 minutes, achieving a maximum heart rate of 140 beats/min. This patient remained asymptomatic without any antiarrhythmic drug during the 3-month follow-up period. Medical management in case of patients showing disabling inappropriate sinus tachycardia refractory, sinus node modification could be considered as an suitable alternative to complete atrioventricular junctional ablation.

Adult↗

[Stress and stress tolerance in chronic heart failure].

BACKGROUND: Exercise intolerance in patients with chronic heart failure (CHF) shows no correlation to the degree of left ventricular dysfunction. This surprising finding has directed attention to peripheral changes in CHF. During the last years several different peripheral factors as determinants of exercise intolerance have been defined, i.e. abnormalities in ventilation, reduced endothelium-dependent vasodilatation of peripheral conduit and resistance vessels, and altered skeletal muscle metabolism. Skeletal muscle alterations are characterized by a reduced oxidative capacity, a catabolic state with reduced local IGF-I expression and muscle atrophy, chronic inflammation with local expression of the inducible isoform of nitric oxide synthase (iNOS) and an accelerated rate of programmed cell death (apoptosis). EFFECTS OF PHYSICAL EXERCISE: Physical exercise training has evolved as an important therapeutic approach to influence these non-cardiac causes of exercise intolerance. After the first studies documenting the effect of aerobic training on the peripheral causes of exercise intolerance in CHF the question was asked: Should we treat the heart or the periphery to improve exercise intolerance in CHF? Today, we have come closer to the answer: It is now clear that these two systems are not mutually exclusive. Exercise training in CHF has been shown to improve skeletal muscle metabolism and function, to avert muscle catabolism, to reduce neurohumoral overactivation, to reverse endothelial dysfunction and to contribute to the prevention of pathologic left ventricular remodeling. After 6 months of regular exercise training oxidative capacity of the working skeletal muscle increases by approximately 40%. Regular exercise training leads to a significant improvement of endothelium-dependent vasodilatory capacity of peripheral resistance vessels, thereby reducting peripheral resistance in particular during exercise. These beneficial training effects result in a small, but significant improvement of stroke volume and reduction in cardiomegaly. CONCLUSION: Although several questions regarding patient selection, optimal training protocol and training intensity remain unanswered, exercise training can been seen as an established adjunct to pharmacotherapy in CHF. We may soon reach the conclusion that by treating the periphery with exercise programs we are in fact treating the heart, as well. All exercise-induced adaptations converge to increase peak oxygen uptake by up to 2 ml/kg.min. For patients in stable CHF on optimal cardiac medication a combination of in-hospital and home-based aerobic endurance training in combination with local muscle strength training seems most promising. Although exercise training offers no causal treatment of CHF, it has great potentials as an adjunct therapy directed at improving exercise tolerance and expanding the physical limits of CHF patients.

Chronic Disease↗

Central and peripheral haemodynamic determinants of effort tolerance in patients with heart failure.

We studied central and peripheral hemodynamics and exercise tolerance in 24 patients with left ventricular dysfunction. All were in NYHA class II or III, and echocardiographic left ventricular ejection fraction was < 35% without pharmacologic influences. Patients underwent to treadmill test (Naughton protocol), cardiopulmonary upright bicycle test, and supine bicycle test with haemodynamic measurements. All tests were exhaustive. Average exercise time was 9 +/- 3.4 min, (range 3-20). Average ejection fraction (.28 +/- 0.65) dis not correlate with working capacity (r = .32), nor did left ventricular filling pressure (pulmonary capillary wedge pressure) at rest and at peak exercise (r = .29 and r = .02). Stroke volume and stroke volume index were on average depressed, with no variations during work; cardiac output and cardiac index were also depressed, with a significant increase at peak exercise (both p < .001). Systemic and pulmonary resistances were increased, but systemic resistances tended to decrease during effort (p < .001), while pulmonary resistances did not (p = NS). We subdivided patients according to systemic vascular resistances lower or higher than 1500 dynes.cm.sec-5 at rest; this identifies two different working capacities (low systemic vascular resistances 11.7 +/- 4.4 min, high systemic vascular resistances 6.9 +/- 3.2 min, p < .05). Patients were then divided in two groups: group I (rest stroke volume > 60 ml) and group II (rest stroke volume < 60 ml). Group I worked 11 +/- 5 min, group II 8.5 +/- 3 min (p < .05). We performed a linear regression analysis between cardiac output and systemic vascular resistances at rest and during exercise in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Changes in pulmonary function test and cardio-pulmonary exercise capacity in COPD patients after lobar pulmonary resection.

OBJECTIVE: Pulmonary Function Tests (PFT) and Cardio-Pulmonary Exercise Testing (C-PET) are useful to evaluate operability in functionally compromised patients. Although modifications of PFT and C-PET after lung surgery have been widely explored, little information exists as to modifications of exercise capacity in COPD patients undergoing lung resection. We prospectively analyzed the changes in PFT and C-PET in patients with COPD after a pulmonary lobar resection. METHODS: From January 2003 to March 2004 all patients scheduled for lung resection were considered for participation in the study protocol. Those patients with a preoperative diagnosis of COPD on PFT were explored through a C-PET. Only patients who had undergone a lobar pulmonary resection were subsequently considered; these patients had a new complete cardio-respiratory evaluation 3 months after surgery. The pre- and postoperative values compared were those of FEV1, TLC, DLCO, VO2max, and VE/VCO2. Data are expressed as mean +/- standard deviation (SD). Statistic evaluation was made using the Wilcoxon test. RESULTS: During this period 11 patients completed the study protocol. Ten patients underwent surgery for NSCLC and one for a pulmonary aspergilloma. Nine lobectomies and two bilobectomies were performed. In the study population, the preoperative mean value of FEV1 resulted as being 53% (SD+/-20) of the predicted mean value, that of TLC 120% (SD+/-35) and that of DLCO 65% (SD+/-27). The preoperative mean value of VO2max resulted as being 17.8 ml/Kg/min (SD+/-3.25) and mean VE/VCO2 resulted as being 35.7 (SD+/-4). Three months after surgery the measured mean value of FEV1 was 53% (SD+/-18), that of TLC was 99% (SD+/-24) and that of DLCO 52% (SD+/-18). The mean value of VO2max resulted as being 14.1 ml/Kg/min (SD+/-3.04) and that of VE/VCO2 was 42.5 (SD+/-12.8). Statistical analysis of PFT values showed that FEV1 and DLCO were not significantly modified (P > 0.05); in contrast, TLC had significantly decreased (P = 0.008). VO2max had significantly decreased (P = 0.004) and VE/VCO2 had significantly increased (P = 0.018). CONCLUSIONS: Three months after a lobar pulmonary resection, patients with COPD were found to have a significant decrease in exercise tolerance. PFT alone can underestimate the postoperative loss of exercise capacity through exercise.

Aged↗