Management of Pulmonary Artery Synovial Sarcoma: The 3-Step Surgical Approach.

Primary pulmonary artery sarcoma is an uncommon neoplasm. Given its clinical and radiographic resemblance to pulmonary embolism, initial diagnostic steps may be complicated, leading to delay in diagnosis. This report presents the case of a 52-year-old-woman who was admitted with pulmonary embolism. She underwent pulmonary embolectomy, and histopathologic examination revealed synovial sarcoma.

A neglected symptom of contained aortic laceration--dysphagia aortica successfully treated by endovascular stentgrafting.

PURPOSE: Dysphagia aortica describes an esophageal swallowing disorder caused by external compression from an ectatic, tortuous, or aneurysmal thoracic aorta. Although well recognized among specialists, dysphagia aortica is rarely considered in the differential diagnosis of dysphagia. CASE REPORT: We present the case of a 75-year-old woman with a history of swallowing difficulty and retrosternal pressure sensation. Her symptoms had been attributed to sliding axial hernia along with gastroesophageal reflux disease for the last 12 months. Diagnostic workup at our institution revealed a giant penetrating ulcer of the descending aorta as a culprit of esophageal compression. Expeditious endovascular stentgraft exclusion of the aneurysm was performed because of its symptomatic nature and high propensity of spontaneous rupture. On a recent consultation 2 years after the endovascular procedure, the patient confirmed a complete remission of impaired swallowing and freedom from thoracic discomfort. CONCLUSIONS: Dysphagia aortica should be considered in the numerous differential diagnoses of esophageal swallowing disorders in the elderly, as delayed identification may harbor catastrophic outcome for affected individuals.

Gender is an important determinant of the disposition of the loop diuretic torasemide.

Signals from pharmacovigilance studies indicate that women are at higher risk for adverse drug reactions (ADRs) due to diuretics. Despite the long-term use of torasemide, there are few studies investigating gender differences of torasemide pharmacokinetics in the hospital setting. Therefore, torasemide pharmacokinetics were investigated in 90 patients (45 women, 45 men) during steady-state conditions. Torasemide elimination was significantly reduced in women compared with men (eg, body-weight-normalized area under the concentration-time curve: 42.1 +/- 20.4 vs 30.9 +/- 10.3 kg.h/L; P < .001). Among the investigated genetic factors [SLC22A11(OAT4), SLCO1B1(OATP1B1), CYP2C9], only the SLCO1B1c.521T>C polymorphism had a significant influence on torasemide pharmacokinetics. Using cell lines expressing OATP1B1, the authors identified torasemide as OATP1B1 substrate (K(m) = 6.2 microM) with a significant reduction of uptake by the 521C-variant. Taken together, gender differences in torasemide pharmacokinetics are likely to contribute to a higher rate of ADRs in women, which has, for example, been observed in a German Pharmacovigilance Project with 66% of hospitalizations due to torasemide ADRs occurring in women.

Early achievement of mild therapeutic hypothermia and the neurologic outcome after cardiac arrest.

BACKGROUND: Mild therapeutic hypothermia (MTH) achieved by endovascular cooling has emerged as a new treatment strategy to reduce hypoxic brain injury after cardiac arrest (CA). It remains to be established how the time interval between CA and MTH impacts the neurologic outcome. We hypothesized that a more rapid achievement of MTH (time to target temperature [TTT], time to coldest temperature [TCT]) improves the outcome after CA. METHODS: Forty-nine consecutive patients successfully resuscitated from CA were enrolled. MTH with a body core temperature between 32.0 and 34.0 degrees C (target temperature: 33.0 degrees C) over 24 h was achieved using a closed-loop endovascular system. Based on the neurologic outcome at discharge, the patient group was dichotomized into good (no/mild cerebral disability) and poor (severe disability, coma/vegetative state, brain death) outcomes. Serum neurone specific enolase (NSE) as biochemical marker of brain damage was sampled at 24, 48, and 72 h after CA. RESULTS: Twenty-eight patients were discharged with a good outcome. Multivariate stepwise regression showed TTT (odds ratio for every h TTT: 0.69 [95% confidence interval: 0.51-0.98]) or, if entered into the model, TCT (odds ratio for every h TCT: 0.72 [95% confidence interval: 0.56-0.94]) to be independent predictors for good outcome. Further independent determinants were age, BMI, asystole as presenting rhythm, and thrombolysis during resuscitation. However, TCT was the only variable to correlate with maximum NSE values after CA (r=0.32, P<0.05). CONCLUSIONS: Early achievement of MTH by endovascular cooling appears to reduce hypoxic brain injury and to favour a good neurologic outcome after CA.

Determinants of steady-state torasemide pharmacokinetics: impact of pharmacogenetic factors, gender and angiotensin II receptor blockers.

BACKGROUND: Torasemide is frequently used for the treatment of hypertension and heart failure. However, the determinants of torasemide pharmacokinetics in patients during steady-state conditions are largely unknown. We therefore explored the impact of genetic polymorphisms of cytochrome P450 (CYP) 2C9 (CYP2C9) and organic anion transporting polypeptide (OATP) 1B1 (SLCO1B1), gender, and the effects of losartan and irbesartan comedication on the interindividual variability of steady-state pharmacokinetics of torasemide. PATIENTS AND METHODS: Twenty-four patients receiving stable medication with torasemide 10 mg once daily and with an indication for additional angiotensin II receptor blocker (ARB) treatment to control hypertension or to treat heart failure were selected. Blood samples were taken before torasemide administration and 0.5, 1, 2, 4, 8, 12 and 24 hours after administration. After this first study period, patients received either irbesartan 150 mg (five female and seven male patients aged 69+/-8 years) or losartan 100 mg (two female and ten male patients aged 61+/-8 years) once daily. After 3 days of ARB medication, eight blood samples were again collected at the timepoints indicated above. The patients' long-term medications, which did not include known CYP2C9 inhibitors, were maintained at a constant dose during the study. All patients were genotyped for CYP2C9 (*1/*1 [n=15]; *1/*2 [n = 4]; *1/*3 [n=5]) as well as for SLCO1B1 (c.521TT [n=13]; c.521TC [n=11]). RESULTS: Factorial ANOVA revealed an independent impact of the CYP2C9 genotype (dose-normalized area under the plasma concentration-time curve during the 24-hour dosing interval at steady state [AUC(24,ss)/D]: *1/*1 375.5+/-151.4 microg x h/L/mg vs *1/*3 548.5+/-271.6 microg x h/L/mg, p=0.001), the SLCO1B1 genotype (AUC(24,ss)/D: TT 352.3+/-114 microg x h/L/mg vs TC 487.6+/-218.4 microg x h/L/mg, p<0.05) and gender (AUC(24,ss)/D: males 359.5+/-72.2 microg x h/L/mg vs females 547.3+/-284 microg x h/L/mg, p<0.01) on disposition of torasemide. Coadministration of irbesartan caused a 13% increase in the AUC(24,ss)/D of torasemide (p=0.002), whereas losartan had no effect. CONCLUSION: This study shows that the CYP2C9*3 and SLCO1B1 c.521TC genotype and female gender are significant and independent predictors of the pharmacokinetics of torasemide. Coadministration of irbesartan yields moderate but significant increases in the torasemide plasma concentration and elimination half-life.

Impact of enhanced external counterpulsation on peripheral circulation.

Enhanced external counterpulsation (EECP) is a noninvasive counterpulsation technique that reduces angina and improves exercise capacity in patients with coronary artery disease. Diastolic coronary perfusion is augmented by pneumatic compression of 3 sets of cuffs wrapped around the lower extremities. Although central hemodynamic changes are well investigated, almost no data exist about the changes of peripheral circulation during EECP. In this study, 12 patients with angina and angiographic evidence of coronary artery disease were treated for 1 hour with EECP. In these patients, peripheral artery disease was excluded by duplex sonography. The patients rested 1 hour before EECP in supine position, and they remained in that position for 1 hour after the procedure. Changes of flow volumes and flow pattern of the posterior tibial artery and the brachial artery were measured by sonography at the end of all 3 periods. Furthermore, we measured the concentration of circulating prostanoids at these 3 time points. Averaged flow volume of the posterior tibial artery decreased to 69% +/- 23% (P < .05) during EECP and increased to 133% +/- 34% (P < .05) of baseline 1 hour after the procedure. In contrast, the averaged flow volume of the brachial artery increased by 9% +/- 4% (P < .05) during EECP and returned to baseline values after EECP. The flow pattern of the posterior tibial artery showed a second early diastolic antegrade flow caused by the cuff inflation and a reverse end-diastolic flow after the deflation of the cuffs. These flow changes caused an increase of the pulsatility index by Gosling (397% during EECP), returning to baseline values in the recovery period. Plasma concentrations of circulating prostanoids showed no significant change during EECP. Thus, pedal flow volume decreased to approximately two thirds of baseline during EECP followed by reactive hyperemia even 1 hour after the procedure; however, this decreased perfusion triggered no change of the prostacyclin/thromboxane ratio and was well tolerated by all investigated patients. The observed 4-fold increase of the peripheral pulsatility index supports the thesis of increase of shear-stress-related improvement of endothelial function during EECP.

Severe septic inflammation as a strong stimulus of myocardial NT-pro brain natriuretic peptide release.

BACKGROUND: Septic shock (SS) has recently been identified as stimulus of N-terminal pro-brain natriuretic peptide (NT-proBNP) release. We tested whether SS mediates NT-proBNP release through cardiomyocyte necrosis. Moreover, the discriminative value of NT-proBNP for the distinction between SS and non-septic shock (NSS) was assessed. METHODS: The study included 50 ICU patients with SS (n=25) and NSS (n=25), 40 patients with acute coronary syndrome and elevated troponin-I (ACStrop+) and 16 patients with unstable angina and normal troponin-I (UAtrop-). Eleven subjects without inflammation or cardiac disease served as controls. NT-proBNP levels of coronary patients were measured on admission, those of ICU patients 48 h after onset of shock symptoms. RESULTS: ACStrop+ (1525 [25th-75th percentile: 790-3820] pg/L) and NSS (687 [254-1552]) patients showed increased NT-proBNP levels above those of UAtrop- patients (107 [43-450], p<0.001) and controls (52 [42-99], p<0.001), but SS patients exhibited still higher levels (11,335 [4716-25,769], p<0.001 vs all others). Among ICU patients with shock symptoms, NT-proBNP discriminated SS and NSS with high sensitivity and specificity (area under ROC curve: 0.946 [95% confidence interval, 0.872-1.019]). NT-proBNP correlated with troponin-I, as marker of cardiomyocyte damage, among ACStrop+ (p<0.001) and SS patients (p=0.013). But, whereas SS patients showed the greatest NT-proBNP values, ACStrop+ patients had higher troponin-I levels (p<0.001), suggesting different mechanisms by which myocardial ischemia and SS mediate NT-proBNP release. CONCLUSIONS: SS is a more potent stimulus of NT-proBNP release than myocardial ischemia. NT-proBNP reliably distinguishes SS from other forms of shock. SS-related NT-proBNP release appears to involve cardiomyocyte damage but not genuine cardiomyocyte necrosis.

Acute reversible cardiomyopathy with cardiogenic shock in a patient with Addisonian crisis: a case report.

A 42 year-old female, admitted to the ICU, with Addisonian crisis developed acute cardiopulmonary failure after hydrocortisone therapy was initiated. An echocardiogram showed severe reduction in the left-ventricular ejection fraction. Additionally, profound ECG abnormalities with diffuse ST-elevation and decreased QRS-amplitudes occurred, whereas Troponin-I was only moderately increased. Chest X-ray displayed bilateral pulmonary edema. The patient's condition culminated in respiratory failure and cardiogenic shock requiring catecholamines and ventilatory support. After a week, she had recovered uneventfully.

Effect of selective cyclooxygenase-2 inhibitors on heart rate in healthy young men.

During an investigation of the possible pharmacokinetic interactions of cyclooxygenase-2 (COX-2) inhibitors with metoprolol, we observed that rofecoxib caused a significant reduction in heart rate in young healthy volunteers. The effect of valdecoxib did not reach significance. When these drugs were given together with metoprolol, the effect was continued. The latter effect could not be related to pharmacokinetic interactions. In the light of experimental results claiming a cardioprotective effect of possibly COX-2-derived prostaglandins and clinical observations hinting at an increased risk of sudden cardiovascular death in conjunction with the long-term use of selective cyclooxygenase inhibitors, our results may help to increase awareness and to suggest investigation of the impact of coxibs on heart function.

Enhanced external counterpulsation: a new technique to augment renal function in liver cirrhosis.

BACKGROUND: Advanced liver cirrhosis is characterized by cardiovascular changes, such as low arterial blood pressure, peripheral vasodilation and renal vasoconstriction. As a consequence, renal hypoperfusion, impaired diuresis and natriuresis and eventual hepatorenal syndrome may ensue. Previous studies using head-out water immersion to increase central blood volume have demonstrated the functional nature of the renal abnormalities. Enhanced external counterpulsation (EECP) is a new non-invasive cardiac assist device to augment diastolic blood pressure by electrocardiogram-triggered diastolic inflation and deflation of cuffs wrapped around the lower extremities. We investigated whether EECP would improve renal dysfunction of liver cirrhosis. METHODS: Twelve healthy controls and 19 patients with liver cirrhosis were observed during 2 h of baseline followed by 2 h of EECP. The following parameters of renal and cardiovascular function were measured: renal plasma flow by para-aminohippurate clearance, glomerular filtration rate (GFR) by inulin clearance, urine flow rate, urinary excretion rates of sodium and chloride, mean arterial blood pressure (MAP), renal vascular resistance (RVR) and plasma concentrations of renin, atrial natriuretic peptide (ANP), endothelin-1, antidiuretic hormone, epinephrine and N-epinephrine. RESULTS: EECP was well tolerated by healthy controls and cirrhotic patients alike. EECP increased MAP (cirrhotic patients: from 74+/-18 to 88+/-20 mmHg, P<0.01; controls: from 89+/-8 to 94+/-5 mmHg, P = NS) and ANP (cirrhotic patients: from 23+/-18 to 30+/-20 ng/l, P<0.05; controls: from 11+/-4 to 16+/-5 ng/l, P<0.01). The plasma renin concentration decreased (cirrhotic patients: from 98+/-98 to 58+/-57 ng/l, P<0.01; controls: from 4.6+/-1.6 to 3.4+/-1.1 ng/l, P<0.01). This was associated with improvement of the urinary flow rate (cirrhotic patients: from 3.6+/-1.8 to 4.6+/-0.7 ml/min, P<0.05; controls: from 1.8+/-1.5 to 2.8+/-1.9 ml/min, P<0.05), as well as of the sodium and chloride excretion rates in both groups. However, in contrast to healthy controls, GFR and renal plasma flow in cirrhotic patients failed to rise significantly. Renal vascular resistance fell numerically in healthy controls (68+/-5 vs 55+/-4 mmHg . min/l; P = NS). In contrast, RVR showed a significant increase by approximately 20% in cirrhosis (67+/-4 vs 80+/-8 mmHg . min/l; P<0.05). Endothelin-1 levels fell in controls (0.38+/-0.42 vs 0.31+/-0.35; P<0.05), whereas they remained statistically unchanged in cirrhotic patients. Epinephrine, N-epinephrine and vasopressin were not altered by EECP in either group. CONCLUSIONS: EECP is an effective procedure to augment renal excretory function in healthy volunteers as well as in patients with cirrhosis. In healthy volunteers, GFR and renal plasma flow increased during EECP. In contrast, these parameters remained unchanged in the patients and their renal vascular resistance increased during EECP. Therefore, EECP improves diuresis, but does not influence the vasoconstrictive dysregulation of the kidneys in liver cirrhosis.

A liquid chromatography-mass spectrometry method for the quantification of both etoricoxib and valdecoxib in human plasma.

A practicable and selective liquid chromatography-mass spectrometry assay for the determination of two cyclooxygenase-2 inhibitors, etoricoxib and valdecoxib, in human plasma is presented. The analytical technique is based on reversed-phase high-performance liquid chromatography (HPLC) coupled to atmospheric pressure chemical ionisation (APCI) mass spectrometry (Finnigan Mat LCQ ion trap). Mass analysis was performed in the positive ion mode. The ion trap was operated in the tandem MS mode (MS2) and the transitions of etoricoxib (m/z 359.2 --> 280.3) and valdecoxib (m/z 315.1 --> 235.1) were followed by selected reaction monitoring. Retention times of etoricoxib and valdecoxib were 1.05 and 1.08 min, respectively. The method was validated over a linear range 10-2500 and 5-1000 microg/L using the other substrate as internal standard. After validation, the method was used to study the pharmacokinetic pro fi le of etoricoxib or valdecoxib in a healthy volunteer after administration of a single oral dose (valdecoxib, 20 mg; etoricoxib, 90 mg). The presented method was suf fi cient to cover more than 90% of the area under the plasma concentration time curve.

Effect of amiodarone on the plasma levels of metoprolol.

On average, metoprolol plasma concentration is doubled after an amiodarone loading dose (1.2 g/day over a period of 6 days). However, the individual amount of this drug interaction depends on the CYP2D6 genotype.

Accelerated reperfusion of poorly perfused retinal areas in central retinal artery occlusion and branch retinal artery occlusion after a short treatment with enhanced external counterpulsation.

BACKGROUND: To date, no satisfactory therapy has become available for patients with acute central retinal artery occlusion (CRAO) or branch retinal artery occlusion (BRAO). Enhanced external counterpulsation (EECP) is a new noninvasive procedure that increases perfusion of inner organs. In the current study, the authors measured the impact of EECP on reperfusion in ischemic retinal tissue. METHODS: In a prospective, randomized study, 20 patients with CRAO or BRAO were included. Ten patients were given hemodilution therapy and 2 hours of EECP, and 10 patients were given regular hemodilution therapy only. Quantification of changes in retinal perfusion was carried out by means of scanning laser Doppler flowmetry (in arbitrary units). RESULTS: Enhanced external counterpulsation caused no observable adverse events. A significant increase in perfusion occurred immediately after EECP in the ischemic retinal areas (57 +/- 19 arbitrary units versus 99 +/- 14 arbitrary units). In contrast, no change was measured in the group not treated with EECP (83 +/- 19 arbitrary units versus 89 +/- 44 arbitrary units). Forty-eight hours later, a significant increase in perfusion could be shown in the ischemic retina of both groups, and no significant difference of perfusion was found between the two groups any longer. CONCLUSION: The current study suggests that EECP could be a clinically useful and safe procedure in patients with CRAO or BRAO to accelerate recovery of perfusion in ischemic retinal areas.

Single-dose nimodipine normalizes impaired retinal circulation in normal tension glaucoma.

PURPOSE: Several studies indicate that calcium channel blockers improve the clinical course of normal tension glaucoma (NTG), whereas the underlying mechanism is not fully investigated. Hemodynamic improvement and neuroprotective effects are discussed. In this study, we measured the hemodynamic effects of nimodipine on retinal circulation. PATIENTS AND METHODS: Sixteen patients with NTG and clinical signs of vasospastic hyperreactivity, such as suffering from extremely cold hands and feet, were consecutively selected out of the local glaucoma registry. Ten healthy age-matched volunteers were included as controls. Retinal capillary blood flow was measured by Scanning Laser Doppler Flowmetry in both eyes before and 90 +/- 10 minutes after a single oral dose of 30 mg nimodipine. RESULTS: Before administration of nimodipine, retinal capillary blood flow was significantly reduced in NTG patients compared with controls (262 +/- 80 vs. 487 +/- 164 AU, P < 0.001). Nimodipine increased retinal capillary blood flow in NTG patients by 91 +/- 73% (P < 0.001) to values of healthy controls (440 +/- 113 vs. 439 +/- 123 AU, P = 0.635). In controls, nimodipine did not show significant effects. CONCLUSIONS: In NTG patients with additional vasospastic symptoms, retinal capillary blood is significantly reduced in comparison with healthy controls. Single-dose nimodipine yields to a normalization of retinal circulation in NTG patients up to values of healthy controls 90 minutes after drug administration.

Practicability and limitations of enhanced external counterpulsation as an additional treatment for angina.

BACKGROUND: An increasing number of clinical studies indicates reduction of angina and myocardial ischemia by enhanced external counterpulsation (EECP) therapy. However, given the wide range of contraindications and the long duration of treatment, eligibility and practicality issues have not been addressed systematically. HYPOTHESIS: Of all candidates for EECP (patients with drug-refractory angina without possibility of revascularization), the majority either have contraindications or have practical problems complying with the time demands that this therapy imposes. In the rest, EECP leads to satisfactory results. METHODS: During 18 months, every consecutive patient with angina despite medical and interventional therapy was evaluated for EECP at one center. Treated patients underwent a bicycle exercise test and perfusion imaging before and after the standard course of 35 h of EECP. In addition, patients were asked about frequency of angina and nitroglycerin usage before and after EECP, and all patients filled out a final questionnaire 1 year after the end of therapy. RESULTS: Overall, 48 patients were considered candidates for EECP. Of these, 24 were excluded for medical reasons: poor ejection fraction (4), peripheral artery disease (4), anticoagulation (4), and atrial fibrillation (3). Eight further patients declined EECP for lack of time or accommodation. Another 3 of the 16 remaining patients dropped out because of side effects. In the 13 patients who finished the treatment course, weekly anginal episodes were reduced by 48% (p < 0.05), on-demand nitroglycerin puffs were reduced by 51% (p < 0.05), work capacity was improved by 22% (p < 0.05), and the number of reversible perfusion defects in perfusion scans decreased nonsignificantly (-28%). However, 4 of 13 treated patients determined 1 year later that the detriment of loss of time exceeded the benefits of EECP. CONCLUSION: Similar to previous reports, our study confirms the reduction of angina and improvement of work capacity after EECP. However, using established contraindications, approximately two-thirds of patients considered to be candidates had to be excluded, and one-third of the treated patients regarded EECP therapy retrospectively as too time consuming.

Celecoxib inhibits metabolism of cytochrome P450 2D6 substrate metoprolol in humans.

OBJECTIVE: In vitro data have shown that celecoxib inhibits the metabolism of cytochrome P450 (CYP) 2D6 substrates. However, very limited data are available on the influence of cyclooxygenase 2 inhibitors on the disposition of CYP2D6 substrates in humans. Therefore the objective of this study was to examine the effect of celecoxib and rofecoxib on the pharmacokinetics of the clinically relevant CYP2D6 substrate metoprolol. METHODS: An open, randomized, 3-period crossover study was performed in 12 healthy male volunteers. Metoprolol (50 mg) was given in all 3 periods without or after 7 days of pretreatment with celecoxib (200 mg twice daily) or rofecoxib (25 mg daily) to achieve steady-state conditions of cyclooxygenase 2 inhibitors in periods 2 and 3. RESULTS: Celecoxib significantly increased the area under the plasma concentration-time curve of metoprolol from 271 to 414 micro g. h/L (64% +/- 57%, P <.001) and by more than 200% in 1 volunteer. The extent of this drug interaction was more pronounced in volunteers with 2 fully functional alleles compared with volunteers with 1 fully functional allele (103% +/- 75% versus 36% +/- 23%, P <.05). After administration of celecoxib, the area under the plasma concentration-time curve from 0 to 24 hours of alpha-hydroxymetoprolol decreased significantly from 474 to 387 micro g. h/L (P <.01). Rofecoxib caused no significant effects on the pharmacokinetics of metoprolol. CONCLUSION: We conclude that celecoxib inhibits the metabolism of the CYP2D6 substrate metoprolol but that rofecoxib does not. Clinically relevant drug interaction may occur between celecoxib and CYP2D6 substrates, particularly those with a narrow therapeutic index.

Increased hypoxic blood pressure response in patients with amyotrophic lateral sclerosis.

OBJECTIVES: There is evidence of impaired cardiovascular autonomic control and reduced baroreflex sensitivity in patients with amyotrophic lateral sclerosis (ALS). A compromised baroreflex-chemoreflex interaction might result in inadequate responses to chemoreflex activation with progressive hypercapnia and hypoxia and contribute to early fatalities. This study was performed to assess cardiovascular and ventilatory responses to hypercapnic and hypoxic stimulation in ALS patients with impaired baroreflex function. PATIENTS AND METHODS: In 15 ALS patients with previously demonstrated baroreflex dysfunction and in 15 age-matched controls, we compared electrocardiographic RR-interval (RRI), systolic blood pressure (SBP) and minute ventilation (VE) during normal ventilation and during selective progressive hypoxia and hypercapnia. RESULTS: Ventilatory and RRI responses to hypoxic and hypercapnic stimulation as well as SBP responses to hypercapnia did not differ between patients and controls. In contrast, hypoxia induced a significant SBP increase in patients only. CONCLUSIONS: The normal ventilatory and RRI responses to chemoreflex activation suggest intact afferent chemoreflex function. The hypertensive response to hypoxia might be due to a compromised interaction with the baroreflex. Avoiding hypoxic episodes might reduce the risk of cardiovascular crisis in ALS patients.

Incidence and characteristics of segmental postsystolic longitudinal shortening in normal, acutely ischemic, and scarred myocardium.

OBJECTIVE: Myocardial longitudinal shortening after aortic valve closure (postsystolic shortening [PSS]) is considered a marker of pathology with diagnostic potential. However, PSS can also occur in healthy subjects. We, therefore, investigated the occurrence and characteristics of PSS in control subjects and patients, and how to distinguish normality from disease. METHODS: In 20 young control subjects, 10 older control subjects, 30 patients with acute myocardial infarction (acute ischemia), and 10 patients with postischemic myocardial scar, longitudinal myocardial deformation was measured with Doppler tissue strain rate (SR) imaging. Segmental SR and strain were visually and quantitatively analyzed and compared. RESULTS: In young control subjects, PSS was found in 98 of 313 segments (31%) and showed gaussian distribution (median 1.3%). During ejection time, median peak SR was -1.4 s(-1) and median strain -16.6%. In older control subjects, parameters differed only slightly. In acutely ischemic and scarred myocardium, both systolic strain and SR were significantly reduced or inverted. In disease, PSS occurred significantly more often (78% and 79%, respectively), was significantly higher in magnitude, and its peak occurred later than in young and older control subjects. CONCLUSION: PSS is a normal finding in healthy subjects occurring in approximately one-third of myocardial segments and, thus, is not always a marker of disease. Our data indicate that pathologic PSS can be detected by coexisting reduction in systolic strain and, second, by exceeding a postsystolic strain magnitude cutoff.