Evidence of unbalanced regulatory mechanism of heart rate and systolic pressure after acute myocardial infarction

2002 ◽  
Vol 283 (3) ◽  
pp. H1200-H1207 ◽  
Author(s):  
Giandomenico Nollo ◽  
Luca Faes ◽  
Alberto Porta ◽  
Barbara Pellegrini ◽  
Flavia Ravelli ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Feedforward Control ◽  
Systolic Pressure ◽  
Systolic Arterial Pressure ◽  
Surrogate Data ◽  
Control Mechanisms ◽  
Partial Recovery ◽  
Head Up Tilt ◽  
Young Subjects

The interactions between systolic arterial pressure (SAP) and R-R interval (RR) fluctuations after acute myocardial infarction (AMI) were investigated by measures of synchronization separating the feedback from the feedforward control and capturing both linear and nonlinear contributions. The causal synchronization, evaluating the ability of RR to predict SAP (χs/t) or vice versa (χt/s), and the global synchronization (χ) were estimated at rest and after head-up tilt in 35 post-AMI patients, 20 young and 12 old. Significance and nonlinearity of the coupling were assessed by surrogate data analysis. Tilting increased the number of young subjects in which RR-SAP link was significant (from 17 to 19) and linear (from 11 to 18). In AMI, both significance and linearity of the coupling were low at rest (26 significant and 24 nonlinear) and further reduced after tilt (17 significant and 16 nonlinear). Old subjects showed a partial recovery of linearity after tilt (rest: 1 linear of 7 significant; tilt: 5 linear of 8 significant). In young subjects, the causal synchronization indexes were balanced and increased from rest (χt/s= 0.072 ± 0.037 and χs/t = 0.054 ± 0.028) to tilt (χt/s = 0.125 ± 0.071 and χs/t = 0.108 ± 0.053). On the contrary, in old subjects and AMI patients, the feedforward was prevalent to the feedback coupling at rest (old: χt/s = 0.041 ± 0.023 and χs/t = 0.069 ± 0.042; AMI: χt/s = 0.050 ± 0.030 and χs/t = 0.089 ± 0.053). Tilting blunted the unbalance in old subjects (χt/s = 0.065 ± 0.052 and χs/t = 0.069 ± 0.044) but not in AMI patients (χt/s = 0.040 ± 0.019 and χs/t = 0.060 ± 0.040). Thus, after AMI, nonlinear mechanisms are elicited in RR-SAP interactions. Furthermore, the neural regulation of the cardiovascular system resulted in imbalance as a consequence of impaired feedback and enhanced feedforward control mechanisms.

Exploring directionality in spontaneous heart period and systolic pressure variability interactions in humans: implications in the evaluation of baroreflex gain

2005 ◽  
Vol 288 (4) ◽  
pp. H1777-H1785 ◽  
Author(s):  
Giandomenico Nollo ◽  
Luca Faes ◽  
Alberto Porta ◽  
Renzo Antolini ◽  
Flavia Ravelli
Keyword(s):  
Spectral Analysis ◽  
Spectral Component ◽  
Systolic Pressure ◽  
Low Frequency ◽  
Systolic Arterial Pressure ◽  
Phase Lag ◽  
Healthy Humans ◽  
Head Up Tilt ◽  
Causal Approach ◽  
Young Subjects

Although in physiological conditions RR interval and systolic arterial pressure (SAP) are likely to interact in a closed loop, the traditional cross-spectral analysis cannot distinguish feedback (FB) from feedforward (FF) influences. In this study, a causal approach was applied for calculating the coherence from SAP to RR ( Ks-r) and from RR to SAP ( Kr-s) and the gain and phase of the baroreflex transfer function. The method was applied, compared with the noncausal one, to RR and SAP series taken from 15 healthy young subjects in the supine position and after passive head-up tilt. For the low frequency (0.04–0.15 Hz) spectral component, the enhanced FF coupling ( Kr-s = 0.59 ± 0.21, significant in 14 subjects) and the blunted FB coupling ( Ks-r = 0.17 ± 0.17, significant in 4 subjects) found at rest indicated the prevalence of nonbaroreflex mechanisms. The tilt maneuver recovered FB influences ( Ks-r = 0.47 ± 0.16, significant in 14 subjects), which were stronger than FF interactions ( Ks-r = 0.34 ± 0.19, significant in 9 subjects). At the respiratory frequency, the RR-SAP regulation was balanced at rest ( Ks-r = 0.30 ± 0.18 and Kr-s = 0.29 ± 0.20, significant in 11 and 8 subjects) and shifted toward FB mechanisms after tilt ( Ks-r = 0.35 ± 0.19 and Kr-s = 0.19 ± 0.11, significant in 14 and 8 subjects). The causal baroreflex gain estimates were always lower than the corresponding noncausal values and decreased significantly from rest to tilt in both frequency bands. The tilt-induced increase of the phase lag from SAP to RR suggested a shift from vagal to sympathetic modulation. Thus the importance of nonbaroreflex interactions pointed out the necessity of accounting for causality in the cross-spectral analysis of the interactions between cardiovascular variables in healthy humans.

Platelet-activating factor antagonism and streptokinase-induced hypotension in clinical acute myocardial infarction

2001 ◽  
Vol 100 (6) ◽  
pp. 601-607 ◽  
Author(s):  
Roger TAYLOR ◽  
Daniel FATOVICH ◽  
Thomas HITCHCOCK ◽  
Catherine MORRISON ◽  
Lloyd CURTIS
Keyword(s):  
Myocardial Infarction ◽  
Blood Pressure ◽  
Acute Myocardial Infarction ◽  
Receptor Antagonist ◽  
Platelet Activating Factor ◽  
Systolic Pressure ◽  
Induced Hypotension ◽  
Paf Receptor ◽  
Double Blinded ◽  
Paf Receptor Antagonist

Continuing efforts are being made to improve thrombolytic therapy for acute myocardial infarction (AMI). The rate of streptokinase (SK) infusion is commonly limited by the hypotension that is induced. If this could be avoided, an accelerated regimen of SK could be given, analagous to that used for other thrombolytic agents such as alteplase. The mechanism of the SK-induced hypotension is unknown, but there is some evidence that platelet-activating factor (PAF) plays a role. The potent PAF receptor antagonist lexipafant (10 mg) (n = 35), or matching placebo (n = 36), was administered intravenously over 5 min, in a randomized double-blinded protocol, to consecutive patients about to receive SK for AMI; all but three had inferior MI, because of the preference for strategies other than SK therapy in patients with anterior MI. The rate of infusion of SK was set to give 1.5×106 units over 30 min, anticipating significant hypotension. Blood pressure fell sharply over the first 10 min of SK administration. The maximum fall in systolic blood pressure occurred between 8 and 12 min, and averaged 43±28 mmHg (mean±S.D.) and 40±26 mmHg in patients given placebo and lexipafant respectively. Systolic pressure having fallen to < 90 mmHg, according to protocol the SK administration rate was reduced in 21 of 36 (58%) of patients given placebo and in 19 of 35 (54%) of patients given lexipafant. The total SK dose was given to all subjects over 40.3±17.5 and 40.2±13.4 min for the placebo and lexipafant groups respectively. Peak and time integrals of creatine kinase were not different in the two groups. There were no adverse effects attributable to lexipafant. It is concluded that the PAF receptor antagonist lexipafant has no significant effect on SK-induced hypotension and does not facilitate an accelerated regimen of administration.

scholarly journals Prognostic Analysis for Cardiogenic Shock in Patients with Acute Myocardial Infarction Receiving Percutaneous Coronary Intervention

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Mao-Jen Lin ◽  
Chun-Yu Chen ◽  
Hau-De Lin ◽  
Han-Ping Wu
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Percutaneous Coronary Intervention ◽  
Cardiogenic Shock ◽  
Systolic Pressure ◽  
Coronary Intervention ◽  
Syntax Score ◽  
Long Term Outcome ◽  
Percutaneous Coronary ◽  
All Cause Mortality

Cardiogenic shock (CS) is uncommon in patients suffering from acute myocardial infarction (AMI). Long-term outcome and adverse predictors for outcomes in AMI patients with CS receiving percutaneous coronary interventions (PCI) are unclear. A total of 482 AMI patients who received PCI were collected, including 53 CS and 429 non-CS. Predictors for AMI patients with CS including recurrent MI, cardiovascular (CV) mortality, all-cause mortality, and repeated-PCI were analyzed. The CS group had a lower central systolic pressure and central diastolic pressure (both P<0.001). AMI patients with hypertension history were less prone to develop CS (P<0.001). Calcium channel blockers and statins were less frequently used by the CS group than the non-CS group (both P<0.05) after discharge. Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) score, CV mortality, and all-cause mortality were higher in the CS group than the non-CS group (all P<0.005). For patients with CS, stroke history was a predictor of recurrent MI (P=0.036). CS, age, SYNTAX score, and diabetes were predictors of CV mortality (all P<0.05). CS, age, SYNTAX score, and stroke history were predictors for all-cause mortality (all P<0.05). CS, age, and current smoking were predictors for repeated-PCI (all P<0.05).

scholarly journals Acute kidney injury with cardiorenal syndrome; experience from a tertiary care renal unit in Pakistan

2020 ◽  
Vol 10 (4) ◽  
pp. e29-e29
Author(s):  
Rubina Naqvi
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Acute Kidney Injury ◽  
Infective Endocarditis ◽  
Cardiac Failure ◽  
Kidney Injury ◽  
Congestive Cardiac Failure ◽  
Fluid Replacement ◽  
Partial Recovery

Introduction: Acute kidney injury (AKI) is a commonly recognized clinical problem after many morbid conditions related to heart like congenital heart disease surgery, acute or chronic congestive heart failure, acute myocardial infarction, infective endocarditis or cardiomyopathies. Cardio-renal syndrome (CRS) includes a spectrum of disorders involving both the heart and kidneys simultaneously; here acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other. Objectives: To report here, case series of patients with AKI developing in association with CRS. We aim to report different causes of CRS and outcome of patients in this group of patients. Patients and Methods: Subjects for the study reported here comprised a cohort of 34 patients coming to this institution with AKI in association of CRS. AKI was defined according to KDIGO guidelines and CRS based on consensus conference of ADQI in 2012. Type 1or type2 CRS are included in the study. All patients had normal size kidneys on ultrasonography. Results: Thirty-four patients with AKI and CRS were brought to this institute from January 1990 to December 2014; this was contributing 1% to medical causes of total AKI. Among these 25 were males and 9 females; mean age of these patients was 54.06±14.106 years. Causes of CRS were acute myocardial infarction (ST elevated), congestive cardiac failure, infective endocarditis and dilated cardiomyopathy. More than two third of patients were either oliguric or anuric on presentation. Fluid replacement and/or inotropic support required in 79%. Renal replacement therapy in form of hemodialysis was conducted in 64.7% and intermittent peritoneal dialysis in one patient. Complete renal recovery was observed in 19 (56%) patients, while 12 (35%) died during acute phase of illness. CKD-V developed in one patient, 2 patients lost long term follow up, but became dialysis free and renal functions were in improving trends, they were labeled as partial recovery. Secondary insults like hypotension, aggressive diuresis, and volume loss from gastro-intestinal tract or infection were evaluated for any co-relation with outcome but statistically no significant difference was found. Conclusion: CRS can be severe life-threatening condition especially when patients present with circulatory collapse. Diuretics must be used cautiously in patients with congestive cardiac failure. Infective endocarditis with acute right heart failure can lead to CRS.

scholarly journals SYSTOLIC FUNCTION AND DYSSYNCHRONY IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION

2013 ◽  
Vol 4 (2) ◽  
pp. 4-11
Author(s):  
N A Yaroschuk ◽  
V V Kochmasheva ◽  
V P Dityatev ◽  
O B Kerbikov
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Pulmonary Hypertension ◽  
Normal Values ◽  
Systolic Function ◽  
Systolic Pressure ◽  
Control Group ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
Group Standard Deviation

Echographic evaluation of systolic function plays an important role in examination of the patients with acute myocardial infarction (AMI). Recent developments in real-time 3D echocardiography (RT3DE) allow us to evaluate additional parameters such as the dyssynchrony.The aim of this study was to evaluate the relationship between myocardium dyssynchrony and systolic function and to assess the prognostic value of dyssynchrony and its influence on the development of arrhythmias and fatal event in post AMI period.Methods: Study population consisted of 82 (mean age 52±21) patients with AMI and 65 age and gender matched persons with similar cardiovascular risk factors, but without AMI (control group). Standard deviation of the time to the regional LV minimum systolic volume for all 16 segments Tmsv4 16-SD index was used for the assessment of dyssynchrony. The follow-up period was 6 months afterAMI.Results: Tmsv 16-SD values were significantly higher in patients with MI compared control group (6.8 ± 2.7% vs 2.9 ± 1.6 % respectively, р<0,001). Moderate negative correlation was observed between Tmsv 16-SD and Cardiac Index (CI) (r =-0.58, p<0.008). No significant correlations were found between Tmsv 16-SD and mean arterial pressure and herat rate. Tmsv 16-SD was significantly lower in patients with pulmonary hypertension (maximum systolic pressure in lung artery (SPLA) – 55.0±5.58 mm Hg) as compared to patients without pulmonary hypertension (maximum SPLA – 33.0±5.76 mmHg); 4.9±0.75 vs 6.1±1.88 respectively, р=0.03. Significant positive correlation was observed between Tmsv 16-SD and end-diastolic volume (EDV) (r=0.63; р<0.05) and negative with ejection fraction (EF) (r=-0.73; p<0.05).28 patients (34%) of the MI group had the increase Tmsv 16-SD and normal values of EDV and EF. According to ROC analysis ROC Tmsv 16-SD>6.1 was associated with arrhythmic complications in post IM period (sensitivity 83.3%, specificity 87.5%, AUC=0.865, p<0.0001). Tmsv 16SD>6.1 correlates with increasing likelihood of fatal event (sensitivity 87.5%, specificity 71.6%, AUC=0.81, p<0.0001)Conclusions: Tmsv 16-SD is increased in patients with MI. In 34% of MI patients the increase of Tmsv 16-SD was observed in combination normal values of EF and EDV which allow us to consider Tmsv 16-SD as an additional indicator describing pathological changes in myocardium. Tmsv16-SD is correlated with hemodynamic indicators such as CI and SPLA. High Tmsv 16-SD is associated with increased level of arrhythmic complications and fatal events.

Effect of Head-Up Tilt on Subcutaneous Blood Flow during the Course of Acute Myocardial Infarction

1981 ◽  
Vol 60 (2) ◽  
pp. 213-216 ◽  
Author(s):  
K. Skagen
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Blood Flow ◽  
Coronary Occlusion ◽  
Impulse Activity ◽  
Subcutaneous Tissue ◽  
Vasoconstrictor Response ◽  
Head Up Tilt ◽  
Subcutaneous Blood Flow ◽  
133Xe Washout

1. Central and local regulation of subcutaneous blood flow in the forearm was studied in the acute phase of myocardial infarction. 2. Blood flow was measured by the local 133Xe-washout technique. 3. The vasoconstrictor response to increase in venous transmural pressure was not present on day 1 after coronary occlusion but gradually recurred during days 2, 3 and 7. 4. Passive 30° head-up tilt induced a vasoconstriction in subcutaneous tissue. There was no difference in this response at any time during the course of acute myocardial infarction. The vasoconstriction could be blocked by proximal nervous blockade. 5. Thus a decrease in baroreceptor activity induced by head-up tilt enabled a marked neurogenically mediated vasoconstriction in subcutaneous tissue, indicating that orthodromic impulse activity in sympathetic fibres can be further increased even on day 1 of acute myocardial infarction.

Effect of Elevated Pulmonary Artery Systolic Pressure on Short-Term Prognosis in Patients With Acute Myocardial Infarction

Angiology ◽  
2020 ◽  
Vol 71 (6) ◽  
pp. 567-572 ◽  
Author(s):  
Xiao-ting Fan ◽  
Sheng-ji Wang ◽  
Haroon Mujahid ◽  
Xiao-ping Ji
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Pulmonary Artery ◽  
Cardiac Death ◽  
Cox Model ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Future Research ◽  
Characteristic Analysis ◽  
Short Term

Pulmonary artery systolic pressure (PASP) may increase because of cardiac alterations that result in increased filling pressures after acute myocardial infarction (AMI). We hypothesized that PASP might be a useful maker to predict the risk of cardiac death after AMI. We carried out a retrospective study from 2013 to 2017 involving 5401 patients with AMI. Patients were grouped according to their admission PASP result, and the primary end point was cardiac death in 6 months after AMI. Pulmonary artery systolic pressure was associated with age, AMI site, Killip classification, and decreased ejection fraction. After adjustments for clinical and echocardiographic parameters in a Cox model, PASP was found to be significantly related to cardiac death. In receiver operating characteristic analysis, PASP >30 mm Hg had a sensitivity of 59.8% and a specificity of 62.5% for predicting 6-month cardiac death after AMI. In conclusion, PASP at the index admission may be a useful marker predicting short-term cardiac death. These results have implications for future research and management of patients with AMI.

Reduced forearm α1-adrenergic vasoconstriction is associated with enhanced heart rate fluctuations in humans

2006 ◽  
Vol 100 (3) ◽  
pp. 792-799 ◽  
Author(s):  
Shizue Masuki ◽  
John H. Eisenach ◽  
Frank A. Dinenno ◽  
Michael J. Joyner
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Brachial Artery ◽  
Coefficient Of Variation ◽  
Pressure Fluctuations ◽  
Systolic Pressure ◽  
Systolic Arterial Pressure ◽  
Adrenergic Agonist ◽  
Arterial Blood ◽  
Young Subjects

In the present study, we assessed whether heart rate (HR) or arterial pressure fluctuations are enhanced in healthy young humans with reduced α-adrenergic vasoconstrictor responses and, if so, whether this occurs for both α1- and α2-adrenergic receptor-mediated vasoconstriction. Arterial pressure (brachial artery catheter) and HR (ECG) were monitored continuously, and α1- and α2-adrenergic responsiveness was determined by assessing the effects of brachial artery infusions of phenylephrine (α1-adrenergic agonist) and dexmedetomidine (α2-adrenergic agonist), respectively, on forearm blood flow (strain gauge plethysmography). α1-Adrenergic responsiveness varied markedly among the subjects ( n = 20) and was inversely correlated with coefficient of variation for HR ( R2 = 0.37, P < 0.01), whereas the responsiveness was not correlated with the coefficient of variation for either systolic or diastolic arterial pressure. α1-Adrenergic responsiveness was inversely and more strongly correlated with baroreflex sensitivity ( R2 = 0.62, P < 0.0001), determined from beat-to-beat changes in HR and systolic arterial pressure, than the coefficient of variation for HR. On the other hand, α2-adrenergic responsiveness was not correlated with any of the parameters determined above. These results suggest that, in healthy young subjects, the enhanced HR response to changes in systolic pressure helps maintain the stability of arterial blood pressure when α1-adrenergic responsiveness is reduced.

Sign in / Sign up

Export Citation Format

Share Document