BACKGROUND:Since an inverse relationship between percutaneous coronary angioplasty (PTCA) case-load and in-hospital major adverse cardiac events (MACE) exists, we intended to evaluate the performance of low-volume PTCA operators, during the first year of our interventional program, by applying the more accurate index represented by the MACE rate within the first month.METHODS:The data relative to both the PTCA procedure and the control visit 3-4 weeks later, were retrospectively reviewed. Death, myocardial infarction and need for revascularization were the end-points evaluated, both globally and with respect to the individual operators.RESULTS:During 1999, 61 consecutive patients (53M, 8F; mean age: 59.9+/-10.4 years) were treated by two full-trained operators. Stable angina was the indication in 75% of cases. Comorbidities as diabetes and prior revascularization, were present in 16 and 5% of cases, respectively. Multivessel procedures were performed in 33% of cases, with a total number of lesions of 84 (77% A/B1 type). Stents were implanted in 70% of cases, as a bail-out in 12%. Procedural success rate was 93%. Overall one-month MACE rate was 3.3%, accounted for by 1 in-hospital emergency coronary surgery occurred to operator 1 (3.6% one-month MACE rate) and 1 elective coronary operation performed in a stable patient previously treated by operator 2 (3% one-month MACE rate).CONCLUSIONS:PTCA performed in a low-volume center by low-volume operators is not necessarily associated with a poor outcome, provided that adequate selection of low-risk cases is accomplished. Although only 52% of the Italian centers met in 1999 the recommended volume standards, reaching optimal case-load should anyway be pursued. Some time should however be conceded, provided that close monitoring of one-month MACE rate shows adequate performance of both the institution and the operators.

The optimal approach to the diagnosis of acute pulmonary embolism is still controversial. The poor sensitivity and specificity of most of the clinical manifestations, the suboptimal accuracy of the majority of the laboratory and instrumental examinations and the highly variable local availability of the diagnostic resources, makes it in fact difficult for a univocal strategy to be adopted. Recently published practical guidelines, however, support the use of lung scanning (either ventilation/perfusion or only perfusion) as a first-line imaging test, since this approach allows for a correct diagnosis in most patients, after careful history taking, physical examination and electrocardiogram, chest X-ray and arterial blood gas analysis performance. When lung scanning is non-diagnostic, either serial non-invasive (i.e. ultrasonographic) evaluation of the lower limbs or pulmonary angiography should follow. Growing evidence is accumulating on the use of spiral computed tomography scanning either as an alternative or as a complement to lung scanning, while echocardiography should be reserved for the bedside evaluation of critically ill patients, when more validated techniques are not readily available. The role of plasma D-dimer measurement has yet to be defined, especially in hospitalized patients. In current clinical practice, however, these recommendations seem to be only partially followed. Depending in fact on the different characteristics of the populations examined in the seven available studies reporting on this issue, the use of the different diagnostic techniques appears highly variable. Although a standard diagnostic pathway does not seem applicable to all patients with suspected acute pulmonary embolism, further work is nonetheless needed in order to identify in different patient subsets the diagnostic approach capable of minimizing the use of diagnostic resources while obtaining the greatest amount of information.

To determine whether reduced sarcoplasmic reticulum (SR) Ca2+-adenosinetriphosphatase (ATPase) (SERCA2) activity contributes to delayed myocardial relaxation during chronic left ventricular hypertrophy (LVH) progression, LVH was produced in rats by abdominal aortic coarctation. Systolic and diastolic functions were assessed in vivo 8 and 16 wk after surgery, and compositional alterations in LV myocardium [SERCA2 concentration, myosin heavy chain (MHC) isoenzymes, and tissue collagen] were correlated with the development of prolonged isovolumic relaxation and impaired cardiac performance over time. Myocardial relaxation was prolonged in 8-wk banded rats, despite normal isovolumic systolic function and LV end-diastolic pressure (LVEDP). No significant alterations in SERCA2 protein, beta-MHC, or fibrillar collagen levels were observed at this early time point. In contrast, LV SERCA2, beta-MHC, and fibrillar collagen concentrations were all significantly altered in 16-wk banded rats. These late compositional changes were associated with reduced cardiac performance, as manifested by a significant elevation in LVEDP (14 +/- 2 mmHg). The 34% decrease in SERCA2 protein was associated with reduced SR Ca2+ uptake and an even greater reduction (76%) in SERCA2 mRNA. SERCA2 mRNA levels were also significantly reduced to 43 +/- 10% of sham-operated rats 8 wk after banding, despite unchanged SERCA2 protein levels and normal SR Ca2+ uptake. These results argue against a significant contribution of SERCA2 downregulation to the subtle alterations in myocardial relaxation observed in compensated LVH. However, the early reduction in SERCA2 mRNA levels may serve as a molecular marker for impaired cardiac performance during the transition from compensated LVH to heart failure.

We used complex demodulation of cardiac interval and systolic arterial blood pressure oscillations in the low-frequency band (0.04 to 0.14 Hz) to investigate baroreceptor control of heart rate. Baroreflex sensitivity was defined as the instantaneous amplitude of complex-demodulated oscillations in the RR interval divided by the instantaneous amplitude of complex-demodulated oscillations in systolic blood pressure. We evaluated the method using both simulated and actual data obtained from 33 healthy nonsmokers during supine and standing postures. To test the validity and reliability of the method, we compared the mean values of baroreflex sensitivity calculated using complex demodulation with the values obtained using power spectral analysis and sequential analysis of spontaneous variations in blood pressure and RR interval. All three methods applied to the simulated data yielded the same values of baroreceptor sensitivity. Mean values of baroreflex sensitivity assessed by complex demodulation of the actual data were similar to those calculated by both power spectral analysis and sequential analysis (13.9 +/- 5.2 versus 13.7 +/- 6.7 or 14.3 +/- 6.5 ms/mm Hg for supine and 7.3 +/- 2.8 versus 7.0 +/- 3.0 or 7.2 +/- 2.8 ms/mm Hg for standing, respectively). In addition, a significant correlation existed between the values obtained by complex demodulation and power spectral analysis (r = .97, P = .0001) and sequential analysis (r = .98, P = .0001). Furthermore, complex demodulation-derived baroreflex sensitivity fluctuated across time during both the supine and standing postures, and this could not be discerned by power spectral analysis. The results indicate that complex demodulation provides a dynamic assessment of baroreflex sensitivity and may be a useful tool in exploring reflex autonomic control of the cardiovascular system.

Objective: The aim was to investigate me influence of the sympathetic nervous system on the induction of mechanical and electrical alternans in the intact canine heart. Methods: Experiments were performed on 8 open-chest dogs anesthetized with sodium pentobarbital. A micromanometer-tipped catheter was used to measure left ventricular pressure, dp/dt and the time constant of isovolumic relaxation. Rapid atrial pacing was used to induce alternans and the left stellate ganglion was stimulated electrically to alter sympathetic tone. The longest pacing cycle length that showed a significant alternation in peak systolic pressure was defined as the alternans threshold. Electrical alternans was detected by comparing the ST-T area in the surface ECG (lead II) on alternate beats. Results: The alternans threshold was 305(s.e.m. 10.4) ms under control conditions and decreased to 271(12.1), 225(33.4), and 177(6.2) ms, as the frequency of left stellate stimulation was increased to 1, 2, and 5 Hz, respectively (P < 0.001). Tau and peak -dp/dt began to alternate at the same pacing cycle length as peak +dp/dt and peak systolic pressure. Electrical alternans was only observed during mechanical alternans and the ST-T area of the strong beat was 243(143)% greater than the ST-T area of the weak beat (P < 0.001). Timolol (1 mg . kg(-1)) blocked the effect of left stellate stimulation (1 and 2 Hz) on mechanical and electrical alternans. Conclusions: Left sympathetic activation causes a frequency-dependent reduction in the threshold cycle length for global mechanical and electrical alternans. Alternation in relaxation occurs at the same pacing cycle length as does alternation in contraction. Repolarization alternans in the surface ECG appears to reflect underlying mechanical events.

The concentrations of acetone, isoprene, and pentane in alveolar breath were examined in 50 smokers and 50 nonsmokers by gas chromatography. The baseline pentane in smokers was 0.17 +/- 0.03 nmol/L (mean +/- SE), which was not different from pentane in nonsmokers (0.23 +/- 0.03 nmol/L). There were also no differences between smokers and nonsmokers in the concentrations of acetone and isoprene. Serial breath samples were obtained from 15 smokers before smoking and at 5, 15, and 60 min after smoking. Although acetone was not altered by smoking, isoprene increased by 86% +/- 26% 5 min after smoking (P <0.001) and returned to baseline 10 min later. Pentane increased by 456% +/- 156% 5 min after smoking (P <0.001) and remained increased 10 min later (204% +/- 73% of baseline, P <0.05). Isoprene concentrations in mainstream cigarette smoke were >5000 times greater than breath concentrations, whereas pentane could not be detected in mainstream smoke. Because pentane is produced from the peroxidation of n-6 polyunsaturated fatty acids, the results provide evidence that cigarette smoking causes an immediate increase in lipid peroxidation.

The reflex vagal control of atrial repolarization was investigated in eight open-chest, anesthetized dogs. A monophasic action potential was recorded from the right atrium, and the action potential duration to 90% repolarization (APD90) was determined every cardiac cycle. beta-Adrenergic receptors were blocked with timolol (0.1 mg/kg). Under baseline conditions, sinus slowing during sinus arrhythmia was accompanied by a significant shortening of APD90 (24 +/- 4.0 ms). Transient occlusion (30 s) of the descending thoracic aorta increased systolic aortic pressure from 138 +/- 2.8 to 181 +/- 3.3 mmHg (P < 0.01). Heart rate decreased from 99 +/- 3.6 to 42.5 +/- 3.4 beats/min (P < 0.01), and APD90 shortened from 168 +/- 5.1 to 94 +/- 3.3 ms (P < 0.01). Release of the occlusion caused arterial hypotension (95 +/- 2.8 mmHg) and an overshoot in both rate (126 +/- 5.2 beats/min) and APD90 (189 +/- 2.3 ms). Aortic occlusion during atrial pacing (130-160 beats/min) decreased APD90 from 147 +/- 7.0 to 78 +/- 3.4 ms (P < 0.01). Cervical vagotomy or atropine eliminated changes in rate and APD90 evoked by aortic occlusion. The results indicate that there is parallel central vagal control of both sinus rate and atrial repolarization. Sinus bradycardia during reflex vagal activation does not prevent the acceleration of atrial repolarization.

BACKGROUND:Symptomatic improvement of a patient's hemodynamic condition during intraaortic balloon counterpulsation (IABC) is considered to result largely from a reduction in afterload. Afterload can be accurately quantified by arterial input impedance measurements. Here we report the effect of IABC on arterial impedance in humans.METHODS:To characterize the effects of IABC on arterial input impedance, impedance measurements were obtained using aortic annulus Doppler flow and pressure from the aortic balloon catheter. Impedance spectra were compared between the cardiac cycles preceding and following the cycle with IABC in 25 patients.RESULTS:Intraaortic balloon counterpulsation increased stroke volume (23%; p = 0.001), reduced myocardial oxygen demand (11%; p = 0.02), and decreased the aortic pressure at the onset of systole (16%; p = 0.001). There was also a decrease in systemic vascular resistance (24%; p = 0.001), characteristic arterial impedance (21%; p = 0.002), and pulse wave reflection (20%; p = 0.006). Linear regression analysis showed that an increase in stroke volume was predicted only by the decrease in systemic vascular resistance (r = -0.81; p = 0.001).CONCLUSIONS:The reduction in systemic vascular resistance appeared to be the major mechanism by which IABC improved cardiac pumping efficiency. This effect may result from the passive distention of the peripheral vascular bed due to the propagation of the balloon-augmented diastolic pressure through the arterial system.

Objective: The aim was to investigate the influence of the sympathetic nervous system on the native collateral circulation in the intact heart. Methods: Experiments were performed on 10 open chest dogs anaesthetised with or chloralose. The left anterior descending coronary artery was cannulated and embolised with 25 mu m microspheres. Collateral resistance was determined from measurements of aortic pressure and retrograde flow. Additional haemodynamic measurements included left Ventricular pressure and blood flow in the circumflex coronary artery. Results: Coronary embolisation decreased retrograde resistance from 41.5(SEM 6.0) to 20.1(1.9) mm Hg.ml(-1)min(-1) (P<0.01). Left stellate stimulation for 60 s (10 Hz) significantly increased circumflex blood flow and decreased circumflex resistance from 2.1(0.3) to 1.6(0.2) mm Hg.ml(-1).min(-1). Retrograde resistance during sympathetic stimulation decreased from 19.7(1.8) to 16.8(1.8) mm Hg.ml(-1).min(-1) (P<0.01). Transient occlusion of descending aorta resulted in changes in perfusion pressure and retrograde flow that. were similar to those observed during stellate stimulation. Stellate stimulation after beta blockade with timolol (0.1 mg.kg(-1)) increased circumflex resistance from 1.9(0.2) to 2.3(0.3) mm Hg.ml(-1).min(-1) (P<0.01) but did not alter retrograde resistance. Conclusions: The sympathetic nervous system does not have a direct effect on native coronary collateral vessels. Increased sympathetic input to the heart does not result in a coronary steal phenomenon. The primary determinant of flow and resistance in the native collateral network during sympathetic activation is the arterial perfusion pressure.

Pentane and isoprene concentrations were analyzed in single end-expiratory breath samples using gas chromatography. Breath analysis was performed in 15 patients with acute myocardial infarction, 15 patients with stable angina, and 15 healthy control subjects. The two patient groups were well matched for age, sex, smoking habits, hypertension and serum cholesterol levels. There was no significant difference in breath pentane concentration in the acute myocardial infarction group (0.29 +/- 0.03 nmol/l) (mean +/- SEM) compared to the group with stable angina (0.31 +/- 0.03 nmol/l) or the control group (0.36 +/- 0.04 nmol/l). However, breath isoprene concentration was higher (p < 0.01) in the acute myocardial infarction group (11.4 +/- 1.2 nmol/l), compared to both the stable angina group (7.7 +/- 0.5 nmol/l) and the control group (7.1 +/- 1.0 nmol/l). There was no difference in either the pentane or isoprene concentrations between the control group and the group with stable angina, Since pentane is thought to be an index of lipid peroxidation, the results do not support the presence of enhanced lipid peroxidation in acute myocardial infarction in the absence of thrombolytic therapy or primary angioplasty. The mechanism responsible for isoprene elevation in acute myocardial infarction is unknown.

To evaluate the effect of acute myocardial edema (ME) on coronary vascular resistance (CVR) and left ventricular (LV) mechanical function, the LV water content (% of total weight) of seven groups (n = 10 each) of isolated rat heart was determined. Group I included non-perfused hearts and served as control. Group II was perfused with Krebs-Henseleit buffer only for the brief equilibration period which preceded every experiment. Group III, IV and V were perfused for 90 min at the constant pressure of 60, 100 and 140 mmHg respectively. Group VI and VII were perfused for 90 min at the constant flow of 10 and 30 ml/min respectively. The hearts were contracting isovolumically against a fluid-filled latex balloon with fixed volume. CVR and LV functional parameters were measured throughout the whole perfusion period. The water content of Group I (78.2 +/- 0.3%) was significantly lower than Group II (80.5 +/- 0.3%). A higher degree of ME was present in groups III, IV and V (80.2 +/- 0.3, 81.4 +/- 0.3 and 83.3 +/- 0.2%, respectively), as well as in groups VI and VII (80.7 +/- 0.1 and 83.4 +/- 0.2%, respectively). CVR significantly increased over time in groups III, IV and V (about +30, +35 and +50%, respectively), as well as in groups VI and VII (about +22 and +20%, respectively). LV developed pressure did not change over time in Group III (which did not show further fluid accumulation after the equilibration period); it decreased on the other hand in groups IV (about -27%) and V (about -40%). In groups VI and VII, LV developed pressure showed as increase (about +28%) and a reduction (about -29%) respectively. In conclusion, in the isolated crystalloid-perfused rat heart, ME is directly dependent on coronary perfusion pressure and/or flow. ME induces an increase in CVR and a rapid and significant depression of LV function.

Journal Article The effect of cytokineI-n on vascular/myocardial function Get access PAUL A SOBOTKA, PAUL A SOBOTKA Loyola University Medical Center, Maywood, IL60153, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar DAVID E EULER DAVID E EULER Loyola University Medical Center, Maywood, IL60153, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 27, Issue 8, August 1993, Page 1551, https://doi.org/10.1093/cvr/27.8.1551 Published: 01 August 1993