Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Shock”

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 19 recordsLinked to original sources
PubMed1979

Shock as a signal for shock or no-shock: a feature-negative effect in conditioned suppression.

Rats were trained in conditioned suppression discriminations where shock at the beginning of a trial signaled either shock or no-shock at the end of the trial. In the shock-positive condition, shock at the beginning of a presentation of white noise signaled that noise would end with shock; noise that did not begin with shock did not end with shock. In the shock-negative discrimination, shock at the beginning of noise signaled that noise would not end with shock; presentations of noise that did not begin with shock ended with shock. In shock-random training, shock at the beginning of noise did not reliably signal whether the noise presentation would or would not end with shock. Most subjects in shock-negative training quickly developed a differential pattern of suppression on positive (shock reinforced) trials and no suppression on negative (nonreinforced) trials. The shock-positive discrimination was much more difficult to establish and was not acquired by the majority of the rats. This "feature-negative" effect is a clear exception to the general superiority of feature-positive learning commonly observed in discriminations based on a single distinguishing feature. The results are discussed in terms of Pavlovian stimulus-shock contingencies in the shock-positive and shock-negative paradigms, which appear to favor rapid development of the shock-negative discrimination.

Acoustic Stimulation↗
PubMed1966

Free operant avoidance as a function of the response-shock = shock-shock interval.

Two temporal parameters of free operant or Sidman avoidance behavior are the interval by which responses postpone shocks (Response-Shock interval) and the interval between shocks when no responses occur (Shock-Shock interval). Avoidance behavior was examined in three white rats under conditions where the Response-Shock and Shock-Shock intervals were always equal. With intervals from 10 to 60 sec response rates and shock rates were similar, decreasing, negatively accelerated functions of increasing Response-Shock=Shock-Shock interval. Over this range, response and shock rates were linearly related to the reciprocal of the Response-Shock=Shock-Shock interval. It was shown, however, that this relation cannot hold at extremely long intervals. Both the ratio of responses emitted to shocks received and the percentage of shocks possible which were avoided increased at long Response-Shock=Shock-Shock intervals. These findings may be related to the fact that long intervals provide optimal conditions for conditioning avoidance behavior in the rat.

Animals↗
PubMed1970

The response-shock-shock-shock interval and unsignalled avoidance in goldfish.

Goldfish were trained to swim back and forth in a shuttle tank to avoid unsignalled shocks. The response-shock interval and the shock-shock interval were always of equal duration; both were either 15, 30, 45, or 60 sec. Response rates varied inversely with response-shock-shock-shock interval duration, as has been found with rats. Percentage of shocks avoided was somewhat lower at the 15 sec response-shock-shock-shock interval, but otherwise did not vary systematically with changes in the interval. As the response-shock-shock-shock interval increased, the fish made increasingly more responses than necessary to avoid all shocks. Interresponse-time distributions showed that response probability rose to a maximum at about 15 to 25 sec after a response, regardless of the response-shock-shock-shock interval. Thus, at the longer intervals the fish were responding too early in the response-shock-shock-shock interval to minimize response rates.

Journal Article↗
PubMed1995

Transcription of heat shock gene loci versus non-heat shock loci in Chironomus polytene chromosomes: evidence for heat-induced formation of novel putative ribonucleoprotein particles (hsRNPs) in the major heat shock puffs.

The heat shock response of Chironomus polytene chromosomes was reexamined. The in vivo effects of heat shock on chromosomal [3H]uridine labeling, RNA polymerase II distribution and ribonucleoprotein (RNP) formation were investigated. One primary result is a clarification of the number and location of chromosomal sites strongly induced by treatment at 37 degrees C for 60 min. In total, seven major heat shock loci were identified by transcription autoradiography in Chironomus tentans: I-20A, II-16B, II-10C, II-4B, II-1C, III-12B, and IV-5C. Secondly, combining immunofluorescence with transcription autoradiography, I find RNA polymerase II occurring after heat shock at multiple chromosomal sites that were also active under normal conditions (20 degrees C). Furthermore, the results demonstrate conclusively that the presence of RNA polymerase II at heat shock and non-heat shock loci is generally correlated with [3H]uridine labeling during heat shock. These latter results extend and corroborate previous findings. Thirdly, the most striking result of this study was revealed in ultrathin sections of puffs by electron microscopy: I discerned a site-specific ultrastructural difference in putative RNP particles between heat shock versus non-heat shock loci. At least three of the seven induced major heat shock puffs (I-20A, III-12B, IV-5C) were observed to contain globular particles that were different, i.e. significantly larger, 250-1,000 A in diameter with a prominent 500-750 A class, than RNP particles of other loci under non-heat shock conditions. These large heat shock puff particles presumably represent nascent or newly synthesized heat shock RNA associated with protein(s) to form heat shock RNPs (hsRNPs). This finding suggests the possible involvement of novel RNPs (hsRNPs) in transcriptional regulation or heat shock RNA turnover and may stimulate further molecular investigations on this subject in both cell physiological and structural terms. I conclude that the locus-specific putative hsRNPs are an intrinsic property of greatly increased heat shock gene transcription.

Animals↗
PubMed2000

Implications of the timing of onset of cardiogenic shock after acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?

OBJECTIVES: We sought to examine the implications of the timing of onset of cardiogenic shock (CS) after acute myocardial infarction (MI). BACKGROUND: Little information is available about the relationships between timing, clinical substrate, management and outcomes of shock. METHODS: The multinational SHOCK Trial Registry enrolled MI patients with CS from 1993 to 1997. Cardiogenic shock was predominantly attributable to left ventricular (LV) failure in 815 Registry patients for whom temporal data were available. We examined factors related to the timing of shock onset and the relation of temporal onset to in-hospital outcomes. RESULTS: Overall, shock developed a median of 6.2 h after MI symptom onset. Shock onset varied by culprit artery: left main, median 1.7 h; right, 3.5 h; circumflex, 3.9 h; left anterior descending (LAD), 11.0 h; saphenous vein graft, 10.9 h (p = 0.025). Early shock (< 24 h) occurred in 74.1% and was associated with chest pain at shock onset, ST-segment elevation in two or more leads, multiple infarct locations, inferior MI, left main disease and smoking. Late shock (> or = 24 h) was associated with recurrent ischemia, Q waves in two or more leads and LAD culprit vessel. Mortality was higher in patients with early versus late shock (62.6% vs. 53.6%, p = 0.022). CONCLUSIONS: Shock onset after acute MI occurred within 24 h in 74% of the patients with predominant LV failure. Mortality was slightly higher in patients developing shock early rather than later. Many factors influence when shock develops, which has implications for its management.

Aged↗
PubMed1976

Effects of electric-shock delivery on schedule-induced water intake: delay of shock, shock intensity, and body-weight loss.

In each of four experiments, schedule-induced water intake in the rat was studied under fixed-time 40-sec food delivery. Experiments I and II studied the temporal relationship between response-independent electric-shock delivery and licking. Shock was delivered under a variable-time 60-sec schedule. A lick-dependent delay was imposed so that licking and shock delivery were systematically separated in time by a minimum of 1 to 15 sec. Over a wide range of shock intensities the data failed to reveal a consistent delay-of-shock effect. Similar shock intensities led to similar reduction of water intake at each delay of shock interval. Experiments III and IV studied the effects of body-weight loss on water intake during independent shock delivery. In Experiment III, shock was delivered under variable-time 60-sec with a minimum separation between shock and licking of 5 sec. In Experiment IV, shock was delivered under variable-time 180-sec. The minimum separation between shock and licking was 10 sec. In each study, the resistance of water intake to suppression by shock delivery increased as the degree of body-weight loss increased. Schedule-induced water intake was affected more by shock when the animal was maintained at 90% of free-feeding weight than at 70%.

Animals↗
PubMed2003

Heat shock factor 1-independent activation of dendritic cells by heat shock: implication for the uncoupling of heat-mediated immunoregulation from the heat shock response.

The induction of heat shock proteins by heat shock is classically defined as the heat shock response, which is involved in cytoprotection, inflammation and immune responses. Whereas the cytoprotective properties of heat shock have been well characterized, the immunomodulating roles of the heat shock response on the immune system are just emerging. In particular, it is not known whether immunomodulating functions of heat are mediated by the heat shock response. We addressed this question genetically, using a murine model that is unable to mount the heat shock response because of deletion of a major transcriptional factor, heat shock factor 1 (Hsf1). We focused on the roles of heat shock on modulating the functions of dendritic cells (DC) because of their important roles in both innate and adaptive immunity. We found that heat shock matures CD11c(+) DC both in vitro and in vivo, phenotypically and functionally, in the absence of any exogenous inflammatory stimuli. Furthermore, heat-shock-mediated DC maturation is independent of Hsf1, as Hsf1(-/-) DC can be matured by heat shock equally well as wild-type DC. Our novel findings demonstrate that heat shock, one of the most primitive biological responses, can modulate the immune response without the requirement for the transcriptional induction/repression of target genes mediated by Hsf1.

Animals↗
PubMed2000

Intravenous immunoglobulin for treating sepsis and septic shock.

OBJECTIVES: Death from severe sepsis and septic shock is common, and researchers have explored whether antibodies to the endotoxins in some bacteria reduces mortality. This review summarises the effects of intravenous immunoglobulin (IVIG) in patients with bacterial sepsis or septic shock on mortality, bacteriological failure rates, and duration of stay in hospital. SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register, Medline 1966 to April 1999, EMBASE 1988 to February 1999; we contacted investigators active in the field for unpublished data. SELECTION CRITERIA: Randomised trials comparing intravenous immunoglobulin (monoclonal or polyclonal) with placebo or no intervention, in patients with bacterial sepsis or septic shock. DATA COLLECTION AND ANALYSIS: Inclusion criteria, trial quality assessment, and data abstraction were done in duplicate. We conducted pre-specified subgroup analyses by type of immunoglobulin preparation. MAIN RESULTS: Twenty-three out of 49 studies met our inclusion criteria. Overall mortality was reduced in patients who received polyclonal IVIG (n=413; RR=0.60; 95% CI 0.47 to 0.76). Mortality was not reduced among patients who received monoclonal antibodies such as anti-endotoxins (n=1,736 in 4 good-quality studies; RR=0.98; 95% CI 0.86 to 1.12) or anti-cytokines (n=4,318; RR=0.93; 95% CI 0.86 to 1.01). A few studies measured secondary outcomes (deaths from sepsis or length of hospitalisation) but no differences in the intervention and control groups were identified except among those who received polyclonal IVIG, where sepsis-related mortality was significantly reduced (n=161; RR=0.35; 95% CI 0.18 to 0.69). REVIEWER'S CONCLUSIONS: In our opinion, polyclonal IVIG significantly reduces mortality and can be used as an adjuvant treatment for sepsis and septic shock. Adjunctive therapy with monoclonal IVIGs remains experimental.

Humans↗
PubMed1972

Characteristics and response-displacement effects of shock-generated responding during negative reinforcement procedures: pre-shock responding and post-shock aggressive responding.

Bar-pressing (Experiment I) or key-pressing (Experiments II and III) responses of monkeys were reinforced according to a fixed-interval schedule of negative reinforcement: the first response after a fixed interval of time terminated regularly spaced shocks for a fixed time designated as the reinforcement period. During extinction, shocks continued during the reinforcement period. That there were two types of responding generated by shock alone was indicated by (1) the level of responding maintained during extinction relative to conditions without shock, (2) the stability of two between-shock response patterns across reinforcement and extinction conditions, and (3) the development of these two between-shock patterns without a history of reinforcement. Subjects developed either a pre-shock or a post-shock response pattern when only the bar was available. However, when both a bite tube, an operandum requiring an aggressive topography, and a recessed key, an operandum that did not require an aggressive topography, were provided, the post-shock pattern was observed in tube biting and the pre-shock pattern was observed in key pressing. Removal of the bite tube produced post-shock key responding similar to that observed when only the bar was available. The displacement of post-shock, aggression-motivated responding confirmed the confounding effect of shock-generated responding in negative reinforcement procedures, and suggests that the use of concurrent response alternatives would reduce such confounding.

Aggression↗
PubMed2000

Cardiogenic shock complicating acute myocardial infarction--etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?

OBJECTIVES: This SHOCK Study report seeks to provide an overview of patients with cardiogenic shock (CS) complicating acute myocardial infarction (MI) and the outcome with various treatments. The outcome of patients undergoing revascularization in the SHOCK Trial Registry and SHOCK Trial are compared. BACKGROUND: Cardiogenic shock is the leading cause of death in patients hospitalized for acute MI. The randomized SHOCK Trial reported improved six-month survival with early revascularization. METHODS: Patients with CS complicating acute MI who were not enrolled in the concurrent randomized trial were registered. Patient characteristics were recorded as were procedures and vital status at hospital discharge. RESULTS: Between April 1993 and August 1997, 1,190 patients with CS were registered and 232 were randomized in the SHOCK Trial. Predominant left ventricular failure (78.5%) was most common, with isolated right ventricular shock in 2.8%, severe mitral regurgitation in 6.9%, ventricular septal rupture in 3.9% and tamponade in 1.4%. In-hospital Registry mortality was 60%, with ventricular septal rupture associated with a significantly higher mortality (87.3%) than all other categories (p < 0.01). The risk profile and mortality were lower for Registry patients who were managed with thrombolytic therapy and/or intra-aortic balloon counter-pulsation, coronary angiography, angioplasty and/or coronary artery bypass surgery. After adjusting for these differences, the extent to which survival was improved with early revascularization was similar to that observed in the randomized SHOCK Trial. CONCLUSIONS: In this prospective Registry the etiology of CS was a mechanical complication in 12%. The similarity of the beneficial treatment effect in patients undergoing early revascularization in the SHOCK Trial Registry and SHOCK Trial provides strong support for the generalizability of the SHOCK Trial results.

Aged↗
PubMed1991

Attenuation of the heat shock response in HeLa cells is mediated by the release of bound heat shock transcription factor and is modulated by changes in growth and in heat shock temperatures.

When HeLa S3 cells are subjected to a continuous 42 degrees C heat shock, activation of heat shock transcription factor (HSF) and transcriptional activation of the heat shock genes hsp70, hsp89 alpha, and hsp60 is transient, peaking at 40-60 min of heat shock, and then attenuating. We have used in vivo genomic footprinting to demonstrate that attenuation of hsp70 transcription is mediated by release of bound HSF from the heat shock element (HSE) of the hsp70 gene promoter. Release of bound HSF in vivo occurs at a higher rate than would be predicted from in vitro measurements of dissociation. Attenuation of HSF activation and heat shock gene transcription occurs only when mild heat shock temperatures are employed (42 degrees C); increasing the heat shock temperature by 1 degree C elicits a much higher level of activation, which does not attenuate during a 4-hr heat shock. Surprisingly, altering the temperature at which cells are grown prior to heat shock modulates the magnitude and temporal pattern of the response to a given heat shock temperature. This finding suggests that HSF does not sense temperature directly but, instead, may be responsive to the magnitude of the difference between growth and heat shock temperatures.

Base Sequence↗
PubMed1974

Key pecking as a function of response-shock and shock-shock intervals in unsignalled avoidance.

Five pigeons were exposed to an unsignalled avoidance procedure where key pecks were maintained through shock postponement. Functions obtained showed an inverse relationship between rate of responding and length of the response-shock interval, while changes in the shock-shock interval had no systematic effect on response rates. The rate of shocks delivered generally decreased with increases in length of both response-shock and shock-shock intervals. Results show that key pecking in pigeons, maintained through an unsignalled avoidance procedure, was affected by changes in response-shock and shock-shock intervals in the same manner as other responses in pigeons and in rats.

Journal Article↗
PubMed1996

Myocardial vulnerability to T wave shocks: relation to shock strength, shock coupling interval, and dispersion of ventricular repolarization.

INTRODUCTION: Induction of ventricular fibrillation (VF) by T wave shocks is of clinical interest due to the correlation between the upper limit of vulnerability (ULV) and the defibrillation threshold (DFT). However, the ULV has not yet been defined precisely in reference to the entire "area of vulnerability" (AOV), which is defined bifunctionally by both shock strengths and shock coupling intervals, nor has it been related to the dispersion of ventricular repolarization, considered to be an important determinant of vulnerability. METHODS AND RESULTS: In 11 isolated perfused rabbit hearts immersed in a tissue bath containing a 3-lead ECG recording system and two opposite plate electrodes for field shock administration, 7 monophasic action potentials (MAPs) were recorded simultaneously from different epicardial and endocardial regions of the right and left ventricles. An average of 90 +/- 25 monophasic waveform shocks of varying shock strengths and coupling intervals were delivered to each heart to determine the horizontal and vertical boundaries of the AOV. The AOV approximated a rhomboid with homogenous VF inducibility. The ULV and lower limit of vulnerability (LLV) represented discrete corners of the AOV with significant changes in VF inducibility if either shock coupling intervals or shock strength were changed by only 10 msec or 10 V, respectively (P < 0.001). The ULV occurred at 7 +/- 10 msec shorter coupling intervals than the LLV (P < 0.05), and VF-inducing shock strengths at the left corner of the AOV were 50 +/- 67 V higher as compared to the right corner (P < 0.01). The maximal range of VF-inducing coupling intervals coincided (within < 2 msec) with the dispersion of MAPs at 70% repolarization, and the ULV coupling interval coincided (within < 4 msec) with the longest repolarization at 50%. CONCLUSIONS: (1) VF vulnerability to monophasic T wave shocks is defined by an AOV that has the shape of a leftward tilted rhomboid. (2) Both the ULV and LLV are sharply defined upper and lower corners of the AOV rhomboid. (3) The width of the AOV corresponds to the dispersion of ventricular repolarization at the 70% level. (4) Considering the dispersion of ventricular repolarization may yield more precise ULV determinations and a better understanding of the correlation between the ULV and DFT.

Action Potentials↗
PubMed2004

Heat shock-induced dendritic cell maturation is coupled by transient aggregation of ubiquitinated proteins independently of heat shock factor 1 or inducible heat shock protein 70.

The transition of dendritic cells (DCs) from immature to mature states is critical for the optimal priming of the adaptive immune response. This highly regulated process is accompanied by structural and functional alterations of DCs, including rapid and dramatic redistributions of MHC class I and class II molecules to cell surfaces, nuclear translocation of NF-kappaB,and transient appearance of dendritic cell aggresome-like induced structures (DALIS) in the cytosol. We have previously found that DCs can be matured by a non-inflammatory stress stimulation, i.e., heat shock. In this study, we examined if thermomanipulation could induce DALIS formation. We found that heat shock of DCs, but not of other cell types, led to the appearance of aggresome-like structures that were structurally indistinguishable from DALIS induced by lipopolysaccharide (LPS). Furthermore, the induction of DALIS in DCs by heat, but not by LPS, correlated with the increased ability of DCs to cross-present exogenous antigens to MHC I. Since the canonical biochemical response to heat shock is the induction of heat shock proteins (HSP) by heat shock factors (Hsf), we studied the contribution of both HSP and Hsf in heat shock-mediated DALIS formation using gene knockout mice. We demonstrated that neither inducible HSP70 nor the major mammalian heat shock transcription factor Hsf1 was involved in the formation of DALIS. Our results highlighted the important roles of heat shock in modulating the function of DCs, and they further suggested that heat-mediated immune regulation can be uncoupled from heat shock response.

Animals↗
PubMed2004

Transcriptional regulation and binding of heat shock factor 1 and heat shock factor 2 to 32 human heat shock genes during thermal stress and differentiation.

Transcription of mammalian heat shock genes can be regulated by heat shock factors (HSF) 1 and 2. Although it has been shown previously that these factors respond to distinct stimuli, a broad analysis of the induction and function of these factors in living cells has not been performed. In our study, we assayed binding of human HSF1 and HSF2 at the promoters of 32 genes identified through LocusLink as heat shock genes in response to elevated temperature and hemin-induced differentiation in human K562 erythroleukemic cells using the chromatin immunoprecipitation technique. We also measured the induced expression of these genes under these 2 conditions. We found that 17 of the 32 genes were transcriptionally induced during heat shock, and HSF1 binding was detected at 15 of the 17 promoters. Nearly all the genes induced by heat shock were also induced to a lesser degree during hemin treatment. However, some genes were induced significantly more during hemin treatment than during heat shock. A new finding is that HSF1 and HSF2 bind to the same targets, but HSF1 binding is activated more by heat than by hemin treatment, and HSF2 binding is only activated by hemin treatment and not by heat. This technology also identified previously unknown HSF1 binding sites near genes that were previously shown to be heat inducible that may contribute to gene-specific regulation.

Base Sequence↗
PubMed1995

Heat shock protein hsp70 accelerates the recovery of heat-shocked mammalian cells through its modulation of heat shock transcription factor HSF1.

The role of mammalian 70-kDa heat shock protein (hsp70) in regulating cellular response to heat shock was examined by using three closely related rat cells: control Rat-1 cells, thermotolerant Rat-1 (TT Rat-1) cells, and heat-resistant M21 cells, a derivative of Rat-1 cells that constitutively overexpress human hsp70. In all these cells, after a prescribed heat shock, the level of the phosphorylated form of heat shock transcription factor HSF1 and that of HSF1 capable of binding to its cognitive DNA sequence heat shock element (HSE) exhibit similar time dependence. The amount of a constitutive HSE-binding activity (CHBA), on the other hand, inversely correlates with those of the two aforementioned forms of HSF1. The recovery kinetics from heat shock are different for the three cell lines, with the thermal-resistant TT Rat-1 and M21 cells showing faster recovery in terms of the state of phosphorylation of HSF1 and its ability to bind HSE or in terms of the reappearance of CHBA. Treatment with okadaic acid, a serine/threonine phosphatase inhibitor, delays the recovery kinetics of Rat-1 cells but not that of thermal-resistant M21 cells. These results are interpreted in terms of a role for hsp70 in the recovery of heat-shocked mammalian cells.

Animals↗
PubMed2000

Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock?

OBJECTIVES: We sought to compare the characteristics and outcomes of patients with acute myocardial infarction (MI) and cardiogenic shock (CS) caused by rupture of the ventricular free wall or tamponade versus shock from other causes. BACKGROUND: Free-wall rupture is a recognized cause of mortality in patients with acute MI. Some of these patients present subacutely, which provides an opportunity for intervention. Recognition of factors that distinguish them from the overall shock cohort would be beneficial. METHODS: The international SHOCK Trial Registry enrolled patients concurrently with the randomized SHOCK Trial. Thirty-six centers consecutively enrolled all patients with suspected CS after MI, regardless of trial eligibility. RESULTS: Of the 1,048 patients studied, 28 (2.7%) had free-wall rupture or tamponade. These patients had less pulmonary edema, less diabetes, less prior MI, and less prior congestive heart failure (all p < 0.05). They more often had new Q waves in two or more leads (51.9% vs. 31.5%, p < 0.04), but MI location and time to shock onset after MI did not differ. Of patients with rupture or tamponade, 75% had pericardial effusions. No hemodynamic characteristics identified patients with rupture/tamponade. Most patients with rupture/tamponade had surgery and/or pericardiocentesis (27/28); their in-hospital survival rate was identical to that of the group overall (39.3%). Women and older patients with rupture/tamponade tended to survive intervention less often. CONCLUSIONS: Free-wall rupture and tamponade may present as CS after MI, and survival after intervention is similar to that of the overall shock cohort. All patients with CS after MI should have echocardiography in order to detect subacute rupture or tamponade and initiate appropriate interventions.

Aged↗
PubMed2005

Comparison of percutaneous coronary intervention and coronary artery bypass grafting after acute myocardial infarction complicated by cardiogenic shock: results from the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial.

BACKGROUND: The Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial demonstrated the survival advantage of emergency revascularization versus initial medical stabilization in patients developing cardiogenic shock after acute myocardial infarction. The relative merits of coronary artery bypass grafting (CABG) versus percutaneous coronary intervention (PCI) in patients with shock have not been defined. The objective of this analysis was to compare the effects of PCI and CABG on 30-day and 1-year survival in the SHOCK trial. METHODS AND RESULTS: Of the 302 trial patients, 128 with predominant left ventricular failure had emergency revascularization. The selection of revascularization procedures was individualized. Eighty-one patients (63.3%) had PCI, and 47 (36.7%) had CABG. The median time from randomization to intervention was 0.9 hours (interquartile range [IQR], 0.3 to 2.2 hours) for PCI and 2.7 hours (IQR, 1.3 to 5.5 hours) for CABG. Baseline demographics and hemodynamics were similar, except that there were more diabetics (48.9% versus 26.9%; P=0.02), 3-vessel disease (80.4% versus 60.3%; P=0.03), and left main coronary disease (41.3% versus 13.0%; P=0.001) in the CABG group. In the PCI group, 12.3% had 2-vessel and 2.5% had 3-vessel interventions. In the CABG group, 84.8% received > or =2 grafts, 52.2% received > or =3 grafts, and 87.2% were deemed completely revascularized. The survival rates were 55.6% in the PCI group compared with 57.4% in the CABG group at 30 days (P=0.86) and 51.9% compared with 46.8%, respectively, at 1 year (P=0.71). CONCLUSIONS: Among SHOCK trial patients randomized to emergency revascularization, those treated with CABG had a greater prevalence of diabetes and worse coronary disease than those treated with PCI. However, survival rates were similar. Emergency CABG is an important component of an optimal treatment strategy in patients with cardiogenic shock, and should be considered a complementary treatment option in patients with extensive coronary disease.

Aged↗