Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ventricular dysfunction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources
PubMed2006

Subclinical left ventricular dysfunction in migraine attacks.

OBJECTIVE: The aim of the present study was to evaluate cardiac performance of patients with migraine attacks during the overload produced by phenylephrine infusion. Background.-It is known that circulatory changes occur during migraine. However, the relationship between this finding and transient cardiac dysfunction is still unknown. METHODS: By means of two-dimensional direct M-mode echocardiography, we measured fractional shortening, ejection fraction, and mean velocity of circumferential fibers shortening in 18 patients with migraine and in 10 normal subjects as a control group. These measures were performed in two different periods: during attack-free intervals and during attacks. Pain intensity of typical migraine attack was evaluated on a 0 to 10 scale. RESULTS: Cardiac size and function were normal at rest in both groups. However, during migraine attacks, phenylephrine infusion provoked significant decrease in fractional shortening, EF, and mean velocity of circumferential fibers shortening, followed by concomitant increase of headache severity. On the other hand, during the attack-free interval and in the control group phenylephrine infusion did not show significant changes in cardiac function parameters. CONCLUSIONS: Our data suggest that left ventricular dysfunction during the phenylephrine test could participate in the complex pathophysiological mechanism of migraine attacks.

Adult↗
PubMed1992

Left ventricular filling pattern and pulmonary wedge pressure are closely related in patients with recent anterior myocardial infarction and left ventricular dysfunction.

To determine whether mitral flow velocity can be used to estimate mean pulmonary wedge pressure (PWP) in patients with left ventricular dysfunction, 50 patients with recent Q-wave anterior infarction and a reduced ejection fraction (less than 40%) underwent simultaneous pulsed-wave Doppler measurements of mitral flow and right heart catheterization. Doppler tracings and PWP were recorded at rest, after passive leg lifting (45 degrees) and (in 15 patients with increased PWP) after 5 mg sublingual ISDN. Significant correlations were found between the ratio of peak early to peak late diastolic velocity (E/A) and PWP (r = 0.83). Early diastolic deceleration and the ratio of the time velocity integral of atrial contribution to the total time velocity integral were also correlated to PWP (r = 0.80 and r = 0.79 (respectively). The E/A ratio was less than 1 in 25 patients and more than 1 in the remaining 25. An E/A ratio of at least 1 predicted a PWP of more than 20 mmHg with a sensitivity of 100% and a specificity of 86%. In all five patients, in whom the PWP was less than 20 mmHg at baseline and became greater with leg lifting, the E/A ratio changed from less than 1 to more than 1. After ISDN, changes in E/A ratio from more than 1 to less than 1 identified all 12 patients with a PWP falling below 20 mmHg. In conclusion, patients with recent Q-wave anterior infarction and a reduced ejection fraction mitral flow velocity-derived variables correlate with PWP representing a reliable index for the diagnosis of markedly increased PWP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Evaluation of enalapril+losartan treatment with cardiopulmonary exercise test in patients with left ventricular dysfunction.

The aim of this study was to evaluate the effects of the combination of enalapril and losartan in patients with left ventricular systolic dysfunction by means of cardiopulmonary exercise test (CPET). Patients with left-ventricular systolic dysfunction and ejection fractions of 40% or less were included to the study. All patients were under the treatment of enalapril 20 mg once daily. The study group consisted of 20 patients (18 men, 2 women; mean age +/- standard deviation: 62.4 +/-6.5 years) and the comparison group consisted of 10 (8 men, 2 women; mean age 59.3 +/-11.9 years). The dose of 50 mg of losartan once daily was given additionally to the study patients. Breath-by-breath CPET was performed before administration of losartan and then 6-8 weeks later in the study group and 2 times with an interval of 6-8 weeks in the control group without any change in the treatment protocol. In the study group the average exercise times were 361 +/-192 and 454 +/-205 seconds (p = 0.001) before and after the study. Peak oxygen consumption ( VO2) values were 1,209 +/-366 and 1,284 +/-398 mL/minute before and after the study (p = 0.01). Anaerobic threshold VO2 values were 785 +/-187 and 855 +/-217 mL/minute before and after the study, respectively (p = 0.01). Peak heart rates (HR) were 141 +/-28 and 143 +/-22/minute (p = 0.35); peak VO2/HR values were 9.02 +/-3.1 and 9.3 +/-3 mL/minute (p = 0.4) before and after the study, respectively. On the other hand, in the control group, average exercise times were 556 +/-250 and 528 +/-251 seconds (p = 0.8); peak VO2 values were 1,502 +/-537 and 1,450 +/-501 mL/minute (p = 0.2); and anaerobic threshold VO2 values were 1,005 +/-338 and 975 +/-319 mL/min (p = 0.7), before and after the study respectively. At the highest comparable exercise stage for both tests in the study group the expired volume/oxygen consumption ( VE/ VO2) ratio declined from 35.1 +/-6.2 to 32.4 +/-5.6 (p = 0.007). VE values declined from 37.5 +/-10.9 to 33.9 +/-10.1 L (p = 0.02); heart rate declined from 140 +/-27 to 132 +/-21/minute (p = 0.02). No significant change was observed in the mentioned values for the control group. Addition of losartan to the standard therapy in patients with left ventricular systolic dysfunction improved exercise capacity and caused lower heart rate and ventilation requirements for the same exercise level.

Anaerobic Threshold↗
PubMed2002

Impaired coronary flow and left ventricular dysfunction after mechanical recanalization in acute myocardial infarction: role of neurohumoral activation?

BACKGROUND: Reopening of the infarct-related coronary artery is the treatment of choice in the clinical setting of acute myocardial infarction. Nevertheless the removal of the total occlusion obtained either by thrombolysis or by primary angioplasty is followed by the ischemia/reperfusion sequelae. One of many proposed mechanisms playing a role in ischemia/reperfusion damage is a persistent increase in vasoconstrictor tone, which reduces cardiac function and impairs myocardial blood flow during primary percutaneous coronary intervention in acute myocardial infarction (PAMI). METHODS: To investigate early neurohumoral changes during PAMI we enrolled 18 patients, who were collated to 13 patients with stable angina undergoing elective PTCA. To evaluate angiotensin II (AngII), endothelin-1 (ET-1), vasopressin (AVP), norepinephrine (NE), troponin T (TNT), creatinephosphate kinase (CPKM) and isoenzyme MB (CPKMB), we collected blood from the pulmonary artery before and immediately after the infarct-related artery (IRA; TIMI 0 --> 2-3) or culprit lesion revascularization. Hemodynamic and angiographic LV-function parameters were compared to biochemical data. Corrected TIMI-frame count (CTFC) was used as an index of coronary blood flow and correlated to the biochemical measurements. RESULTS: CTFC in the IRA correlated inversely (p = 0.03; r = -0.51) with left ventricular ejection fraction measured after 10 days, and positively (p = 0.03; r = 0.54) with the maximal amount of LDH released after onset of AMI. There was an abrupt and long lasting rise in ET-1 (+65 %; p < 0.001) and an instant short lasting increase in AVP (+37 %; p < 0.05), whereas NE concentrations were elevated prior to PAMI and remained elevated during reperfusion. Correlations with CTFC were found for ET-1 (p = 0.01; r = 0.61) and NE (p = 0.01; r = 0.58) during reperfusion. The extent of left ventricular dysfunction correlated with the concentrations of AVP and NE during reperfusion. CONCLUSIONS: There is evidence for a distinct pattern of neurohumoral activation during early reperfusion in acute myocardial infarction. In particular, we documented substantial increases in AVP and ET-1. Left ventricular wall-stress appears to be involved in the release of AVP. Elevated levels of ET-1 and NE are associated with impaired angiographic reperfusion and increased myocardial damage after mechanical recanalization.

Aged↗
PubMed1995

Comparison of rest-redistribution thallium-201 imaging and reinjection after stress-redistribution for the assessment of myocardial viability in patients with left ventricular dysfunction secondary to coronary artery disease.

Thallium (Tl)-201 reinjection after stress-redistribution (RI) imaging has been proven to accurately identify ischemic and viable myocardium. Quantitative Tl-201 analysis after stress has also shown viable myocardium in most mild to moderate (51% to 85% of normal uptake) irreversible Tl-201 defects. However, if the main clinical question is whether a region is viable, and not whether there is inducible ischemia, a resting protocol may be more appropriate. The aim of this study was to determine whether rest-redistribution (RD) quantitative Tl-201 single-photon emission tomographic imaging provides the same information on viable myocardium as Tl-201 RI. Thus, 15 patients (mean age 58 +/- 9 years) with chronic coronary artery disease and left ventricular dysfunction (ejection fraction 35 +/- 8%) were studied by both RI and RD Tl-201 single-photon emission tomography. Regional Tl-201 uptake was assessed quantitatively using a 16-segment model. When Tl-201 images were classified as normal/reversible (viable) or irreversible (nonviable), RI showed viable myocardium in 145 of 240 myocardial regions (60%), whereas RD showed it in 103 of 240 myocardial regions (43%). The 2 imaging protocols provided concordant information in 176 of 240 myocardial regions (73%). Among the 64 (27%) discordant regions, 53 (22%) were viable by RI and nonviable by RD, whereas 11 (5%) were viable by RD and nonviable by RI (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

The aminotetraline derivative (+/-)-(R,S)-5,6-dihydroxy-2-methylamino-1,2,3,4-tetrahydro-naphthalene hydrochloride (CHF-1024) displays cardioprotection in postischemic ventricular dysfunction of the rat heart.

To analyze the protective effects of the aminotetraline derivative (+/-)-(R,S)-5,6-dihydroxy-2-methylamino-1,2,3,4-tetrahydro-naphthalene hydrochloride (CHF-1024), a compound endowed with DA2-dopaminergic/alpha2-adrenergic receptor agonistic activity, in myocardial ischemia/reperfusion damage. A model of isolated and perfused (15 ml/min) electrically driven (300 beats/min) rat heart subjected to global ischemia (1 ml/min for 20 min) and reperfusion (15 ml/min for 30 min) was followed. Cardiac mechanics changes were evaluated together with biochemical markers of cardiac ischemia in perfusate and tissue tumor necrosis factor-alpha (TNF-alpha). CHF-1024, perfused through the heart for 15 min before ischemia at different molar concentrations (1-100 nM), significantly improved left ventricle developed pressure during reperfusion, and normalized left ventricular end-diastolic pressure and coronary perfusion pressure. This anti-ischemic effect of CHF-1024 was associated to a decrease in creatine kinase and lactate dehydrogenase, both released during heart reperfusion. These events were concomitant with maintenance of a higher production of 6-keto-prostaglandin F1alpha The ability of CHF-1024 to improve postischemic ventricular dysfunction was correlated with a dose-dependent inhibition of the release of both norepinephrine (NE), from sympathetic nerve endings, and TNF-alpha from cardiac tissue. The effect of CHF-1024 on NE release was almost completely antagonized by specific antagonists of presynaptic inhibitory receptors domperidone and rauwolscine. The finding that this new aminotetraline derivative possesses anti-ischemic properties and limits NE release from cardiac nerve endings may bear some therapeutic potential in cardiovascular diseases.

Animals↗
PubMed2003

Noninvasive risk stratification in postinfarction patients with severe left ventricular dysfunction and methodology of the MADIT II noninvasive electrocardiology substudy.

Sudden cardiac death occurs as a result of a complex interplay of changes in myocardial substrate, imbalance of autonomic regulation of the heart, and myocardial vulnerability. Noninvasive electrocardiology serves as a comprehensive tool for investigating factors representing mechanistic pathways leading to cardiac events. Heart rate variability, nonlinear dynamics of heart rate, and heart rate turbulence provide insight into autonomic control of the heart. Prognostic value of these parameters in postinfarction patients is well established for predicting cardiac death, but there is less evidence for their association with sudden death or arrhythmic events. Electrical manifestation of changes in myocardial substrate include QRS and QTc prolongation, presence of conduction disturbances, presence of late potentials, abnormalities of repolarization morphology, and presence of nonsinus rhythm, namely atrial fibrillation. Electrocardiogram (ECG) measures reflecting myocardial vulnerability to arrhythmias include frequent ventricular premature beats, T wave alternans, or QT variability. Prognostic significance of these parameters is documented in studies focused mostly on them as individual markers of risk. The noninvasive electrocardiology substudy of the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II) allows for simultaneous analysis of several of the above ECG markers of risk and will provide insight about relative contribution of mechanistic pathways leading to cardiac death in postinfarction patients with severe left ventricular dysfunction. Combination of a standard 12-lead ECG and 10-minute high-resolution Holter recordings serves to evaluate the prognostic significance of noninvasive electrocardiology parameters for mortality in patients randomized to conventional treatment and for arrhythmic events in patients randomized to implantable cardioverter defibrillator therapy.

Atrial Fibrillation↗
PubMed2004

Food restriction induces in vivo ventricular dysfunction in spontaneously hypertensive rats without impairment of in vitro myocardial contractility.

Cardiac structures, function, and myocardial contractility are affected by food restriction (FR). There are few experiments associating undernutrition with hypertension. The aim of the present study was to analyze the effects of FR on the cardiac response to hypertension in a genetic model of hypertension, the spontaneously hypertensive rat (SHR). Five-month-old SHR were fed a control or a calorie-restricted diet for 90 days. Global left ventricle (LV) systolic function was evaluated in vivo by transthoracic echocardiogram and myocardial contractility and diastolic function were assessed in vitro in an isovolumetrically beating isolated heart (Langendorff preparation). FR reduced LV systolic function (control (mean +/- SD): 58.9 +/- 8.2; FR: 50.8 +/- 4.8%, N = 14, P < 0.05). Myocardial contractility was preserved when assessed by the +dP/dt (control: 3493 +/- 379; FR: 3555 +/- 211 mmHg/s, P > 0.05), and developed pressure (in vitro) at diastolic pressure of zero (control: 152 +/- 16; FR: 149 +/- 15 mmHg, N = 9, P > 0.05) and 25 mmHg (control: 155 +/- 9; FR: 150 +/- 10 mmHg, N = 9, P > 0.05). FR also induced eccentric ventricular remodeling, and reduced myocardial elasticity (control: 10.9 +/- 1.6; FR: 9.2 +/- 0.9%, N = 9, P < 0.05) and LV compliance (control: 82.6 +/- 16.5; FR: 68.2 +/- 9.1%, N = 9, P < 0.05). We conclude that FR causes systolic ventricular dysfunction without in vitro change in myocardial contractility and diastolic dysfunction probably due to a reduction in myocardial elasticity.

Animals↗
PubMed2004

Transcatheter transplantation of autologous skeletal myoblasts in postinfarction patients with severe left ventricular dysfunction.

PURPOSE: To report a case-controlled safety and feasibility study of transcatheter transplantation of autologous skeletal myoblasts as a stand-alone procedure in patients with ischemic heart failure. METHODS: Six men (mean age 66.2+/-7.2 years) were eligible for transcatheter transplantation of autologous skeletal myoblasts cultured from quadriceps muscle biopsies. Six other men (mean age 65.7+/-6.3 years) were selected as matched controls (no muscle biopsies). A specially designed injection catheter was advanced through a femoral sheath into the left ventricle cavity, where myoblasts in solution (0.2 mL/injection) were injected into the myocardium via a 25-G needle. At baseline and in follow-up, both groups underwent Holter monitoring, a 6-minute walk test, New York Heart Association (NYHA) class determination, and echocardiography with dobutamine challenge. RESULTS: Skeletal myoblast transplantation was technically successful in all 6 patients with no complications; 19+/-10 injections were performed per patient (210 x 10(6)+/-150 x 10(6) cells implanted per patient). Left ventricular ejection fraction (LVEF) rose from 24.3%+/-6.7% at baseline to 32.2%+/-10.2% at 12 months after myoblast implantation (p=0.02 versus baseline and p<0.05 versus controls); in matched controls, LVEF decreased from 24.7%+/-4.6% to 21.0%+/-4.0% (p=NS). Walking distance and NYHA functional class were significantly improved at 1 year (p=0.02 and p=0.001 versus baseline, respectively), whereas matched controls were unchanged. CONCLUSIONS: Transcatheter transplantation of autologous skeletal myoblasts for severe left ventricular dysfunction in postinfarction patients is feasible, safe, and promising. Scrutiny with randomized, double-blinded, multicenter trials appears warranted.

Aged↗
PubMed1999

Prognosis in myocardial infarction survivors with left ventricular dysfunction is predicted by electrocardiographic RR interval but not QT dispersion.

OBJECTIVES: The aim of the study was to assess if QT dispersion and RR interval on the standard 12-lead electrocardiogram (ECG) predict cardiac death and late arrhythmic events in postinfarction patients with low left ventricular ejection fraction (LVEF). QT dispersion on a standard electrocardiogram (ECG) is a measure of repolarization inhomogeneity, but its prognostic meaning in myocardial infarction (MI) survivors is unclear, especially in patients with left ventricular dysfunction. RR interval has been shown to predict mortality in post-MI patients, but its prognostic power has not been compared with other noninvasive risk factors. METHODS: Retrospective cohort study. Ninety patients were identified, from a series of 547 consecutive postinfarction patients admitted to our institution for phase II cardiac rehabilitation, as having a LVEF of <0.40 at two-dimensional echocardiography (mean LVEF 0.35+/-0.04; range 0.20-0.39). QT dispersion and RR interval were analyzed on the admission 12-lead electrocardiogram, 20+/-10 (range 8-45) days after MI, using specially designed software. Additional risk markers were collected from clinical variables, signal-averaged ECG and Holter recording. RESULTS: During 24+/-18 (range 1-63) months of follow-up, 10 of 90 patients (11%) died, all from cardiac causes, and there were 18 late arrhythmic events, defined as sudden death or the occurrence of a sustained ventricular arrhythmia > or =5 days after the index MI. QT interval and dispersion were not significantly prolonged in patients who died compared to survivors and not significantly different between patients with and without arrhythmic events. Mean RR interval from standard ECG was significantly shorter in patients with both cardiac death (682+/-99 vs. 811+/-134 ms; P=0.004) and arrhythmic events (720+/-100 vs. 818+/-139 ms; P=0.006). A Cox proportional hazards model identified RR interval from standard ECG (P<0.001) and a history of more than one MI (P=0.002) as significant predictors of cardiac death independent of thrombolytic therapy, LVEF, filtered QRS complex duration at signal-averaged ECG, mean RR and its standard deviation at 24-h Holter monitoring. CONCLUSIONS: Measurement of QT interval and dispersion 3 weeks after MI has no prognostic power in patients with LV dysfunction after a recent MI. RR interval on standard 12-lead ECG is as good a prognostic indicator as other, more expensive, noninvasive markers. These findings may be relevant in this era of limited health care resources.

Chi-Square Distribution↗
PubMed2006

Monocyte chemoattractant protein-1 induces a novel transcription factor that causes cardiac myocyte apoptosis and ventricular dysfunction.

Monocyte chemoattractant protein-1 (MCP-1; CCL2)-mediated inflammation plays a critical role in the development of ischemic heart disease (IHD). However, the gene expression changes caused by signal transduction, triggered by MCP-1 binding to its receptor CCR2, and their possible role in the development of IHD are not understood. We present evidence that MCP-1 binding to CCR2 induces a novel transcription factor (MCP-induced protein [MCPIP]) that causes cell death. Gene microarray analysis showed that when expressed in hiuman embryonic kidney 293 cells, MCPIP induced apoptotic gene families before causing cell death. Mutagenesis studies showed that the structural features required for transcription factor-like activity were also required for causing cell death. Activation of caspase-3 was detected after MCPIP transfection and Z-VAD-fmk partially inhibited cell death. Cardiomyocyte-targeted expression of MCP-1 in mice caused death by heart failure at 6 months of age. MCPIP expression increased in parallel with the development of ventricular dysfunction. In situ hybridization showed the presence of MCPIP transcripts in the cardiomyocytes and immunohistochemistry showed that MCPIP was associated with the cardiomyocyte nuclei of apoptotic cardiomyocytes. CCR2 expression in cardiomyocytes increased with the development of IHD. MCPIP production induced by MCP-1 binding to CCR2 in the cardiomyocytes is probably involved in the development of IHD in this murine model. MCPIP transcript levels were much higher in the explanted human hearts with IHD than with nonischemic heart disease. These results provide a molecular insight into how chronic inflammation and exposure to MCP-1 contributes to heart failure and suggest that MCPIP could be a potential target for therapeutic intervention.

Animals↗
PubMed2000

Independent and incremental prognostic value of (201)Tl lung uptake at rest in patients with severe postischemic left ventricular dysfunction.

BACKGROUND: An elevated (201)Tl lung uptake after stress is related to an adverse prognosis. METHODS AND RESULTS: The functional and prognostic significance of resting (201)Tl lung uptake was assessed in 124 consecutive patients with ischemic heart disease and ejection fraction </=35% undergoing rest-redistribution tomography to evaluate myocardial viability. (201)Tl lung uptake significantly correlated with pulmonary wedge pressure (r=0.66; P:<0.01) and with a restrictive physiology by Doppler echocardiography (P:<0.001). During a 13+/-13-month follow-up, 13 patients died and 23 patients required hospitalization as the result of worsening heart failure or nonfatal myocardial infarction (cumulative events rate 29%). Patients with events had a significantly higher (201)Tl lung/heart ratio (L/H) (P:<0.001). A L/H value >0.61 best separated patients with and without events (ROC area under curve 0.82). Event-free survival was significantly lower in patients with L/H >0.61 (P:<0. 001); L/H >0.61 (chi(2)=10.8; P:<0.001) and a restrictive filling pattern (chi(2)=3.6; P:<0.05) were independent predictors of events. The prognostic value of L/H was incremental over that obtained by clinical, echographic and Doppler data (global chi(2)=20.8). CONCLUSIONS: In patients with severe postischemic left ventricular dysfunction undergoing rest-redistribution (201)Tl imaging, an increased lung tracer uptake showed incremental prognostic value over clinical and other imaging findings, providing clinically useful risk assessment.

Adult↗
PubMedDate not supplied

Baseline/post-nitrate Tc-99m tetrofosmin mismatch for the assessment of myocardial viability in patients with severe left ventricular dysfunction: comparison with baseline Tc-99m tetrofosmin scintigraphy/FDG PET imaging.

BACKGROUND: Positron emission tomography (PET) flow/metabolic mismatch is considered the nuclear medicine gold standard for the assessment of myocardial viability. The aim of this study was to investigate whether baseline/nitrate technetium 99m tetrofosmin single photon emission computed tomography (SPECT) mismatch may provide equivalent clinical information. METHODS AND RESULTS: We studied 23 patients (aged 62 +/- 10 years, 19 men) with previous myocardial infarction (16 anterior, 4 inferior, and 3 anterior plus inferior) and postischemic heart failure (gated SPECT [G-SPECT] ejection fraction, 26% +/- 8%). All patients underwent Tc-99m tetrofosmin G-SPECT at rest and after nitrates (intravenous isosorbide dinitrate, 0.2 mg/mL, 10 mL/h) as well as a fluorine 18 fluoro-2-deoxy-d-glucose (FDG) PET scan. Regional wall motion analysis was performed with quantitative G-SPECT (QGS). Myocardial dysfunction was defined as a regional QGS score of 2 or greater. Regional perfusion was assessed by quantitative perfusion score (QPS) providing percent Tc-99m tetrofosmin uptake in a 20-segment model. Semiquantitative analysis of FDG uptake was performed by use of polar maps generated by Siemens ECAT HR + software. In areas with a perfusion rate lower than 80%, PET viability was identified by a normalized FDG percent uptake/baseline Tc-99m tetrofosmin percent uptake ratio greater than 1.2. We analyzed 460 segments; 298 (64%) were dysfunctional by QGS analysis. Of these, 170 were viable by PET imaging whereas 128 were nonviable. Regional Tc-99m tetrofosmin uptake was higher in viable than in nonviable segments both at rest (60% +/- 24% vs 42% +/- 12%, P <.01) and after nitrates (67% +/- 20% vs 41% +/- 18%, P <.01). According to receiver operating characteristic curve analysis, a cutoff value of 63% for resting as well as post-nitrate G-SPECT provided the highest diagnostic accuracy for the detection of myocardial viability (67% and 72% at rest and after nitrates, respectively). When the same algorithm used for the comparison with PET (normalized nitrate percent uptake/baseline percent uptake) was applied to G-SPECT, we obtained the highest agreement with PET (accuracy, 93%; sensitivity, 95%; specificity, 92%). CONCLUSIONS: In patients with severe left ventricular dysfunction, perfusion data alone, both at rest and after nitrates, do not allow an accurate estimate of myocardial viability. In dysfunctioning segments, the analysis of rest/post-nitrate Tc-99m tetrofosmin mismatch provides results similar to those obtained by PET flow/metabolic mismatch.

Adult↗
PubMed1993

Effects of lisinopril on cardiorespiratory, neuroendocrine, and renal function in patients with asymptomatic left ventricular dysfunction.

OBJECTIVE: To determine the cardiac, renal, and neuroendocrine effects of lisinopril in men with untreated, symptom free left ventricular systolic dysfunction. DESIGN: A randomised, double blind cross over trial with six week treatment periods to compare lisinopril (10 mg/day) and matching placebo. SETTING: Hospital outpatient department. PATIENTS: Patients with pronounced systolic dysfunction on cross sectional echocardiography due to myocardial infarction at least six months previously, without angina and with no or minimal breathlessness. Eighteen men were identified of whom 15 completed the study. INTERVENTIONS: Lisinopril (10 mg) or placebo given once daily by mouth. MAIN OUTCOME MEASURES: Primary: oxygen consumption at peak exercise. Secondary: resting cardiac function as measured by radionuclide ventriculography and echocardiography, renal function estimated radioisotopically, and plasma indices of neuroendocrine activity. RESULTS: Compared with placebo, lisinopril increased (mean (SD)) peak oxygen consumption during exercise (19.8(3.1) ml/kg/min v 21.4(3.2) ml/kg/min; p < 0.003). Lisinopril did not improve indices of cardiac function at rest. It reduced plasma concentrations of angiotensin II (median values 7 pg/ml to 5 pg/ml; p < 0.02), aldosterone (median values 113 pg/ml to 66 pg/ml; p < 0.05) and atrial natriuretic peptide (median values 69 pg/ml to 40 pg/ml; p < 0.04), but noradrenaline and antidiuretic hormone concentrations did not change. Renal blood flow increased and glomerular filtration rate declined. CONCLUSIONS: Even before the onset of heart failure lisinopril improves the cardiopulmonary response to exercise in patients with systolic ventricular dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Predicting significant coronary artery disease in patients with left ventricular dysfunction.

BACKGROUND: Because coronary artery disease (CAD) is a prevalent comorbidity in patients with low ejection function (EF), a number of patients with heart failure undergo diagnostic cardiac catheterization. The objective of this study was to develop a model to assist clinicians in determining the likelihood of CAD before cardiac catheterization. METHODS: This study was a retrospective analysis using the Duke Databank for Cardiovascular Disease. From the databank, 2054 patients who underwent cardiac catheterization between 1992 and 2002 that was preceded by echocardiography with an EF of < 45% were identified. The patients' median age was 63 years, and the median EF was 30%. Patients were considered to have significant CAD if any major epicardial vessel had > or = 75% stenosis. A multivariable model of CAD was generated using stepwise logistic regression. We included demographic, clinical, electrocardiographic, and echocardiographic parameters, including segmental wall motion abnormality. RESULTS: Of the patients who met the criteria, 1184 (58%) had significant CAD and 870 (42%) did not. Significant predictors of CAD, in the order of their ability to predict significant CAD, included history of myocardial infarction, age, diabetes mellitus, Q wave on electrocardiogram, male sex, and segmental wall motion abnormality (all P < .0001). The area under the receiver operating characteristic curve was 0.865. CONCLUSIONS: By using baseline demographic and clinical characteristics, we developed a highly discriminatory diagnostic model for predicting CAD in patients with heart failure. Given the high prevalence of patients without CAD in this cohort, accurate baseline assessment of patients with left ventricular dysfunction for CAD might avoid unnecessary invasive procedures.

Cardiac Catheterization↗
PubMed1985

Scintigraphically detected predominant right ventricular dysfunction in acute myocardial infarction: clinical and hemodynamic correlates and implications for therapy and prognosis.

To determine the clinical and hemodynamic correlates as well as therapeutic and prognostic implications of predominant right ventricular dysfunction complicating acute myocardial infarction, 43 consecutive patients with scintigraphic evidence of right ventricular dyssynergy and a depressed right ventricular ejection fraction (less than 0.39) in association with normal or near normal left ventricular ejection fraction (greater than or equal to 0.45) were prospectively evaluated. All 43 patients had acute inferior infarction, forming 40% of patients with acute inferior infarction, and only eight (24%) had elevated jugular venous pressure on admission. On hemodynamic monitoring, 74% of patients had a depressed cardiac index (less than or equal to 2.5 liters/min per m2), averaging 2.0 +/- 0.05 for the group. Of these, 30% did not demonstrate previously described hemodynamic criteria of predominant right ventricular infarction (right atrial pressure greater than or equal to 10 mm Hg or right atrial to pulmonary capillary wedge pressure ratio greater than or equal to 0.8, or both). The left ventricular end-diastolic volume was reduced to 49 +/- 11 ml/m2 (n = 22) and correlated significantly with the stroke volume index (r = 0.82; p less than 0.0001) and cardiac index (r = 0.57; p = 0.005). The follow-up right ventricular ejection fraction, determined in 33 patients, showed an increase of 10% or greater in 26 (79%), increasing from a mean value of 0.30 +/- 0.06 to 0.40 +/- 0.09 (p less than 0.0001) without a significant overall change in the mean left ventricular ejection fraction (0.56 +/- 0.10 to 0.56 +/- 0.11, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1991

[Identification of viable myocardium in patients with chronic ischemic disease and left ventricular dysfunction: correlations between blood flow, metabolic activity and regional function].

To identify the presence of viable myocardium in areas of severe systolic dysfunction, we studied 22 patients (age 45 to 78 years) with chronic coronary artery disease and left ventricular dysfunction (mean ejection fraction 29 +/- 9%). All subjects underwent thallium-201 single photon emission computed tomography (SPECT), using the reinjection technique, positron emission tomography (PET) with H2(15)O and 18-fluorodeoxyglucose (FDG) to measure regional blood flow and exogenous glucose uptake, respectively, and nuclear magnetic resonance imaging (MRI). From matched transaxial PET, SPECT and MRI tomograms, a total of 290 left ventricular myocardial regions were analyzed. According to the regional wall thickening, measured from MRI, 3 groups of myocardial regions were identified: akinetic-dyskinetic (n = 60), showing either absence of systolic thickening or systolic thinning; hypokinetic (n = 97), showing an absolute wall thickening less than or equal to 2 mm; normal (n = 133), showing an absolute wall thickening greater than 2 mm. Of the 60 akinetic or dyskinetic regions, 3 were normal by SPECT and 37 corresponded to either a total or partially reversible thallium defect: 34 of these 40 regions also showed presence of FDG uptake by PET. The remaining 20 akinetic or dyskinetic regions showed a thallium defect that remained irreversible after reinjection: in 7 of these 20 regions, however, there was evidence of metabolic activity, as expressed by FDG uptake. Thus, 47 (78%) of the myocardial akinetic or dyskinetic regions showed presence of viable tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2002

[Safety of stress echocardiography with dobutamine used in patients with aortic stenosis and left ventricular dysfunction].

THE AIMS: The aim of the study was to assess the safety of dobutamine echocardiography (DE) in patients with aortic stenosis and left ventricular ejection fraction < or = 45%. METHODS: 162 patients (mean age 59 +/- 13, 64% males) with resting transvalvular peak gradient < 70 mmHg underwent standard DE (doses 5-40 micrograms/kg/min) in a multicenter study involving 10 centers from Poland and Hungary. This analysis involves a subset of 39 pts (34 M, 5 F, age 59 +/- 13) identified according to the criterion of EF < or = 45% and mean aortic gradient < or = 35 mmHg. Clinically indicated coronary arteriography was performed in all patients with left ventricular dysfunction. RESULTS: Peak dobutamine dose was 29 +/- 10 micrograms/kg/min. Peak heart rate was 112 +/- 26 bpm. Systolic arterial pressure was 148 +/- 20 mmHg and diastolic pressure 86 +/- 14 mmHg. Transaortic mean gradient and aortic valve area increased 35 +/- 34% and 19 +/- 15% during peak dobutamine dose, respectively. Ejection fraction improved 16 +/- 14%. The test was positive in 17 (43.6%) patients, negative in 11 (28.2%) patients and non diagnostic in 11 (28.2%) patients. There were no deaths, myocardial infarctions or episodes of sustained ventricular tachycardia as a result of DE. The test was terminated when the following conditions were met: Target heart rate (23.%). Left ventricular asynergy (46.2%). Maximal established dose achieved (7.7%). Side effects (20.5%). The most common side effects were ventricular arrhythmias (35.9%), dyspnea (20.5%) and hypotension < 20 mmHg (10.3%). CONCLUSION: Despite frequent side effects, DE can be safely performed in patients with aortic stenosis and depressed left ventricular contractility.

Adult↗