Myocardial Stunning Research Articles

A Review of Neurogenic Stunned Myocardium.

Neurologic stunned myocardium (NSM) is a phenomenon where neurologic events give rise to cardiac abnormalities. Neurologic events like stroke and seizures cause sympathetic storm and autonomic dysregulation that result in myocardial injury. The clinical presentation can involve troponin elevation, left ventricular dysfunction, and ECG changes. These findings are similar to Takotsubo cardiomyopathy and acute coronary syndrome. It is difficult to distinguish NSM from acute coronary syndrome based on clinical presentation alone. Because of this difficulty, a patient with NSM who is at high risk for coronary heart disease may undergo cardiac catheterization to rule out coronary artery disease. The objective of this review of literature is to enhance physician's awareness of NSM and its features to help tailor management according to the patient's clinical profile.

Takotsubo cardiomyopathy: case report

This article reports a clinical case of Takotsubo cardiomyopathy manifest clinically, biochemicaly, electrocardiographically, and echocardiographicalyas acute myocardial infarction. The diagnosis was based on finding intact coronary arteries and rapid positive dynamics of instrumental and laboratory data. Takotsubo cardiomyopathy (CMP) (stress-associated CMP, apical ballooning syndrome) is a rare reversible disease developing after acute emotional and physical stress. Its prevalence is estimated at 1-2% of all cases of acute myocardial infarction. It most commonly affects postmenopausal women. The clinical picture is similar to that of acute coronary syndrome with transient hypo- and akinesiaof apical and middle segments of the left ventricle (LV) in combination with hyperkinesia of its basal myocardial segment in the absence of stenosis or a spasm of coronary arteries. The precise pathophysiology of the disease is unknown; several hypotheses are proposed including enhancedsympathoadrenal activity, catecholamine multivesselepicardial coronary artery spasm, coronary microvascular dysfunction, catecholamine cardiotoxicity and catecholamine-mediated myocardial stunning. The Mayo Clinic diagnostic criteria are most widely used in clinical practice: transient hypokinesia, akinesia, or dyskinesia of left ventricular mid-segments with or without apical involvement; regional wall motion abnormalities extending beyond the region of blood supply of a single epicardialartery; a stressful event oftenbut not always present in the medical history in the absence of obstructive coronary disease or angiographic evidence of acute plaque rupture; new electrocardiographic abnormalities (either ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin 1 level; the absence of pheochromocytoma and myocarditis. Takotsubo cardiomyopathyhas been classified into 3 types based on the involvement of the left ventricle: classical type, reverse type and mid-ventricular type; lesions of right ventricle are also described. Specific treatment of the disease is unavailable, and the main purpose of therapy is normalization of LV systolic function. The prognosis of Takotsubo cardiomyopathyis favorable, complete clinical recovery is observed in 95,5% of the cases, the average time of recovery is between 2 and 3 weeks.

Influence of high doses of atorvastatin on myocardial stanning in acute myocardial infarction

Aim: The study was a comparison of the effect of early administration of high-dose atorvastatin and low dose for acute myocardial infarction with elevation ST (AMI+ST) on myocardial stunning and regional contractility left ventricle (LV)

A brief review of intradialytic hypotension with a focus on survival.

Intradialytic hypotension (IDH), a common complication of ultrafiltration during hemodialysis therapy, is associated with high mortality and morbidity. IDH, defined as a nadir systolic blood pressure of less than 90 mm Hg on more than 30% of treatments, is a relevant definition and is correlated with mortality. Risk factors for IDH include patient demographics, anti-hypertensive medication use, larger interdialytic weight gain, and dialysis prescription features as dialysate sodium, high ultrafiltration rate, and dialysate temperature. A high frequency of IDH events carries a substantial death risk. An ultrafiltration rate >10 mL/h/kg, and even more so >13 mL/h/kg, is highly predictive of cardiovascular and all-cause mortality. Evidence suggests that IDH causes acute reversible segmental myocardial hypoperfusion and contractile dysfunction (myocardial stunning), which can result in long-term loss of myocardial contractility, leading to premature death. IDH also has negative end-organ effects on the brain and gut, contributing to mortality through stroke, and endotoxin translocation with associated inflammation and protein-energy wasting. Given strong association of IDH and dialysis mortality, a paradigm shift to its approach is urgently needed. Randomized controlled trials are required to prospectively test drugs and monitoring devices which may reduce IDH.

Reconsideration of the role of viable myocardium in revascularization

Recent studies on the role of viable myocardium in revascularization are hot spots. The definition of viable myocardium, multimodality imaging in the assessment of myocardial viability, Meta analyses related to the value of viable myocardium in revascularization, prospective randomized trials, and factors affecting the prognosis of patients after revascularization are reviewed in this article. Key words: Myocardial ischemia; Myocardial stunning; Myocardial reperfusion; Trends

Effects of preadmission beta-blockers on neurogenic stunned myocardium after aneurysmal subarachnoid hemorrhage: A meta- analysis

ObjectiveSpontaneous subarachnoid hemorrhage is mostly caused by the rupture of an aneurysm. Neurogenic stunned myocardium (NSM) is one of the most frequent complications caused by aneurysmal subarachnoid hemorrhage (aSAH). The possible pathogenesis of NSM may be that the catecholamine peak resulting from aSAH leads to subendocardial ischemia or coronary artery spasm. We designed this meta-analysis to find out whether beta-blockers (BB) can significantly reduce the incidence of NSM and improve the outcomes of aSAH. Patients and methodsWe systematically searched PubMed, Embase, Cochrane library, Elsevier and Medline from inception to Feb 2016. All studies related to the preadmission beta-blocker with aSAH were included. ResultsThree retrospective studies and 691 patients were included. The incidence of mortality [OR=0.68, 95%CI (0.08–3.50), P=0.57], cardiac dysfunction [OR = 0.55, 95% CI (0.05–6.49), P=0.63], cerebral vasospasm (OR=0.52 95% CI(0.18–2.56), P=0.50] had no statistical difference between the preadmission BB group and no BB group. ConclusionThe preadmission beta-blocker cannot decrease the incidence of mortality, cardiac dysfunction, cerebral vasospasm in patients with aSAH. A further research of the usefulness of preadmission beta-blocker in patients with aSAH will be needed.

Exploring the Pathophysiology of Takotsubo Cardiomyopathy.

The purpose of this review is to explore the pathophysiology of Takotsubo cardiomyopathy by appraising the interplay between myocardial perfusion, function, metabolism, and, particularly, sympathetic innervation. A number of hypotheses have been proposed to explain the pathogenesis of Takotsubo cardiomyopathy, which include (1) catecholamine cardiac toxicity, (2) myocardial sympathetic innervation disruption, (3) coronary vasospasm, (4) myocardial microvascular dysfunction, and (5) aborted myocardial infarction. These proposals are primarily derived from findings of nuclear myocardial perfusion, metabolism, and cardiac sympathetic innervation imaging. Although data in the literature are not necessarily uniform, the two most plausible working postulates for explaining the phenomenon are (1) regional myocardial stunning (due to coronary vasospasm, microvascular dysfunction, or aborted myocardial infarction) and (2) cardiac sympathetic innervation disruption or toxicity. Current data suggest that disturbances of both coronary circulation and neural innervation are associated with the Takotsubo cardiomyopathy: myocardial stunning from transient ischemic attack and sympathetic innervation disruption. It remains to be determined, however, whether the observed leading mechanistic explanations that have gained momentum are merely the sequelae of the disease rather than its primary etiology.

Myocardial Inactivation of Thyroid Hormones in Patients with Aortic Stenosis.

The human heart expresses the type 2 deiodinase (D2) that activates thyroxine (T4) to triiodothyronine (T3). At the same time, the inactivating type 3 deiodinase (D3) has been found in a rat model of right ventricular hypertrophy. It is not known whether the human myocardium metabolizes thyroid hormone. This study examined myocardial thyroid hormone metabolism in patients with aortic valve stenosis (AS) undergoing aortic valve replacement and in patients with coronary artery disease (CAD) undergoing coronary artery bypass grafting surgery. Myocardial thyroid hormone metabolism was assessed by analyzing the difference in serum thyroid hormone levels between the aortic root (incoming blood) and the coronary sinus (outgoing blood) of patients undergoing cardiac surgery. A total of 23 patients with AS and 35 patients with CAD were included. Patients received a pre-surgical echocardiogram, and pre-, during and post-surgical thyroid hormone serum levels were collected in the myocardial and peripheral circulations. Patients with AS exhibited the expected left ventricle (LV) hypertrophy (i.e., 20-30% increase in LV posterior wall and interventricular septum thickness and ∼10% increase in AS in LV diastolic diameter). Immediately before cardiopulmonary bypass, blood flowing through the AS myocardium exhibited a 4.6% reduction in T3 and 6.9% increase in rT3 levels, decreasing the serum T3/rT3 ratio by 9.6%. T4 and thyrotropin serum levels remained similar between the aortic root and coronary sinus. In contrast, no myocardial thyroid hormone metabolism was observed in CAD patients. Notably, the AS myocardium lost the ability to inactivate thyroid hormone after cardiopulmonary bypass, possibly due to myocardial stunning. There is accelerated thyroid hormone inactivation in the AS myocardium, which is likely the result of D3 expression. No evidence to suggest thyroid hormone activation in the myocardium was obtained in the present study.

Comparison of Circulating MicroRNAs and Cardiac Troponin I Following Brief Ischemia‐Induced Myocardial Stunning

ObjectiveOur laboratory has recently shown that a single episode of brief myocardial ischemia leading to reversible stunning is associated with a significant increase in serum cardiac troponin I (cTnI) in swine. The time‐course of cTnI elevation is delayed and reflects myocyte injury associated with apoptosis in the absence of pathological evidence of necrosis or infarction. In the present study, we compared this pattern of cTnI release to that of several circulating microRNAs (miRNAs) that have shown promise as novel biomarkers of myocardial ischemia to determine whether miRNAs are released into the circulation following brief ischemia‐induced stunning.MethodsClosed‐chest propofol‐anesthetized swine (n=8) were subjected to a 10‐minute occlusion of the distal left anterior descending coronary artery (LAD) to produce brief myocardial ischemia without infarction. Serial echocardiography was performed to evaluate left ventricular function before, during, and after ischemia. Circulating plasma concentrations of miR‐1, miR‐133a, miR‐133b, and miR‐499 were measured by quantitative RT‐PCR at baseline as well as 1‐hour and 24‐hours after reperfusion and compared to serum cTnI values detected by a porcine‐specific ELISA. PCR‐derived quantification cycle (Cq) values were normalized to a synthetic control (cel‐miR‐39) that was spiked‐in during RNA extraction and all data were expressed as a fold‐change vs. baseline.ResultsAnterior wall thickening became dyskinetic during LAD occlusion (61±2% to −6±2%, p<0.001) and remained depressed one‐hour after reperfusion (39±4%, p<0.01), indicative of myocardial stunning. An ~5‐fold increase in serum cTnI was observed 1‐hour after reperfusion (from 13±6 to 51±17 ng/L, p<0.05), followed by a marked, ~200‐fold elevation at 24‐hours (1021±574 ng/L, p<0.01 vs. baseline). Similarly, the circulating concentration of all four miRNAs tended to increase between 1‐hour and 24‐hours post‐reperfusion, although relative changes were variable (Figure). For example, miR‐1 was not significantly elevated 1‐hour after reperfusion but tended to be higher at 24‐hours, while miR‐133a and miR‐133b exhibited low, but significantly elevated concentrations at 1‐hour that rose to ~10‐fold higher levels at 24‐hours. The pattern of miR‐499 release was most similar to that of serum cTnI and was characterized by a 7‐fold elevation 1‐hour post‐reperfusion, followed by a large ~500‐fold increase 24‐hours later.ConclusionCirculating concentrations of several miRNAs are increased following a single episode of brief myocardial ischemia‐induced stunning in the absence of pathological necrosis or infarction. The relative magnitude of elevation varies among miRNAs, but the time‐course generally follows a pattern of delayed release that is comparable to that exhibited by cTnI. These results demonstrate that myocyte necrosis is not required for ischemia‐induced release of cardiac miRNAs, which may have implications for the use of circulating miRNAs as biomarkers for the clinical detection of myocardial infarction.Support or Funding InformationFunding Sources: The National Heart Lung and Blood Institute (HL‐055324, HL‐061610, and F32HL‐114335), the National Center for Advancing Translational Sciences (UL1TR001412), the Department of Veterans Affairs (1IO1BX002659) and the Albert and Elizabeth Rekate Fund in Cardiovascular Medicine.

Clinical value of the evolution of left ventricular global strain in anterior myocardial infarction patients treated with emergency percutaneous coronary intervention

To investigate the evolution of left ventricular global strain in anterior myocardial infarction patients treated with emergency percutaneous coronary intervention (PCI). Methods: A total of 54 patients with PCI were enrolled as a PCI group. Forty healthy subjects were enrolled as a control group. Dynamic cardiac images were collected. All of these images were analyzed off-line by velocity vector imaging (VVI) software. N-terminal pro-B-type natriuretic peptide (NT-proBNP) was measured with an electrochemiluminescence immunoassay through the Elecsys 1010/2010 system. Correlation analysis were undertaken between VVI and NT-proBNP levels in blood. Results: In PCI group, only globle longitudinal strain (GLS) was significantly increased 3 day after operation (P<0.05). GLS and globle circumferencial strain (GCS) were markedly increased 6 months after operation (P<0.05). In PCI group, left ventricular GLS 1 d to 6 months after PCI shows positive correlation with lgNT-proBNP levels (r=0.66, P<0.001). GLS value was -12.50% at the 3rd day after operation, indicating the improvment of cardiac function in the first and sixth month after PCI. Conclusion: The change of Left ventricular globle longitudinal systolic function after emergency PCI may be more sensitive to the improvement of myocardial stunning after STEMI reperfusion; GLS value (-12.50%) at the 3rd day after operation predict the improvment of cardiac function in the first and sixth months after PCI.

Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists.

Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality. Reperfusion strategies are the current standard therapy for AMI. However, they may result in paradoxical cardiomyocyte dysfunction, known as ischemic reperfusion injury (IRI). Different forms of IRI are recognized, of which only the first two are reversible: reperfusion-induced arrhythmias, myocardial stunning, microvascular obstruction, and lethal myocardial reperfusion injury. Sudden death is the most common pattern for ischemia-induced lethal ventricular arrhythmias during AMI. The exact mechanisms of IRI are not fully known. Molecular, cellular, and tissue alterations such as cell death, inflammation, neurohumoral activation, and oxidative stress are considered to be of paramount importance in IRI. However, comprehension of the exact pathophysiological mechanisms remains a challenge for clinicians. Furthermore, myocardial IRI is a critical issue also for forensic pathologists since sudden death may occur despite timely reperfusion following AMI, that is one of the most frequently litigated areas of cardiology practice. In this paper we explore the literature regarding the pathophysiology of myocardial IRI, focusing on the possible role of the calpain system, oxidative-nitrosative stress, and matrix metalloproteinases and aiming to foster knowledge of IRI pathophysiology also in terms of medicolegal understanding of sudden deaths following AMI.

A Case of Persistent Right Ventricular Failure after Rapid Decompression of a Large Chronic Pericardial Effusion

A 33-year-old male presented to emergency with right sided pleuritic chest pain, exertional dyspnoea, and lower limb oedema over the preceding 2 months. There were no other significant cardiac or medical problems and no regular medications. He was tachycardic (130bpm) but normotensive, tachypneoic (30 min) with normal saturation. Chest x-ray showed marked cardiomegaly; urgent transthoracic echocardiogram (TTE) demonstrated a very large global pericardial effusion with diastolic RV collapse and echocardiographic evidence of tamponade. Urgent pericardiocentesis removed 2L of straw coloured fluid via the subxiphoid approach. Despite drainage the patient had persistent dyspnoea and was hypotensive. Progress TTE on day 2 showed a moderate (22 mm) residual pericardial effusion with no evidence of tamponade, however the RV was moderately dilated (base 54 mm) with severely impaired segmental systolic dysfunction. The RV basal segment was akinetic with a hyperkinetic mid-apex (McConnell's sign). LV size was normal with mildly impaired systolic function. CTPA showed an incidental large anterior mediastinal mass (10 × 18 × 14 cm) and was highly suspicious for lymphoproliferative disease. There was no pulmonary embolus and no features of pulmonary arterial hypertension apart from dilated RV. Reaccumulation of the pericardial effusion necessitated creation of a pericardial window. Biopsy of the mediastinal mass confirmed Hodgkin's lymphoma (classical nodular sclerosing type). Staging PET and CT abdomen/pelvis showed stage II disease, and treatment with BEACOPP was commenced. This case highlights the importance of gradual decompression of symptomatic pericardial effusion to avoid RV failure which could be caused by myocardial stunning or by a variant reperfusion injury as a consequence of pericardiocentesis.

Limitations and Challenges in Mapping Ventricular Tachycardia: New Technologies and Future Directions.

Recurrent episodes of ventricular tachycardia in patients with structural heart disease are associated with increased mortality and morbidity, despite the life-saving benefits of implantable cardiac defibrillators. Reducing implantable cardiac defibrillator therapies is important, as recurrent shocks can cause increased myocardial damage and stunning, despite the conversion of ventricular tachycardia/ventricular fibrillation. Catheter ablation has emerged as a potential therapeutic option either for primary or secondary prevention of these arrhythmias, particularly in post-myocardial infarction cases where the substrate is well defined. However, the outcomes of catheter ablation of ventricular tachycardia in structural heart disease remain unsatisfactory in comparison with other electrophysiological procedures. The disappointing efficacy of ventricular tachycardia ablation in structural heart disease is multifactorial. In this review, we discuss the issues surrounding this and examine the limitations of current mapping approaches, as well as newer technologies that might help address them.

Magnolol Reduces Renal Ischemia and Reperfusion Injury via Inhibition of Apoptosis.

Magnolol, a constituent of the bark of Magnolia officinalis, has been reported to decrease myocardial stunning and infarct size. In this study, we investigated whether magnolol can reduce renal ischemia and reperfusion (I/R) injury. Renal I/R, induced by a 60-min occlusion of bilateral renal arteries and a 24-h reperfusion, significantly increased blood urea nitrogen (BUN) and creatinine levels, and caused histological damage to the kidneys of rats. Apoptosis, as evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and caspase-3 activation, was significantly increased in the kidneys. Furthermore, serum levels of tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were significantly elevated, while the interleukin-10 (IL-10) level was suppressed. However, intravenous pretreatment with magnolol at doses of 0.003[Formula: see text]mg/kg and 0.006[Formula: see text]mg/kg 10[Formula: see text]min before renal I/R significantly limited the increases of BUN, creatinine, the histological damage, and apoptosis in the kidneys. The increases in TNF-[Formula: see text], IL-1β, and IL-6, and the decrease in IL-10 were also significantly inhibited. Additionally, magnolol increased Bcl-2 and decreased Bax in the kidneys. Phosphorylation of the prosurvival kinases, including Akt and extracellular signal-regulated kinases 1 and 2 (ERK1/2), was elevated, while phosphorylation of the pro-apoptotic mitogen-activated protein kinases, including p38 and c-Jun N-terminal kinase (JNK), was suppressed. In conclusion, magnolol reduces renal I/R injury. The underlying mechanisms for this effect might be related to the prevention of apoptosis, possibly via the inhibition of both extrinsic and intrinsic apoptotic pathways, including the reduction of TNF-[Formula: see text] production and the modulation of pro- and anti-apoptotic signaling elements.

Beta Blockade and Clinical Outcomes in Aneurysmal Subarachnoid Hemorrhage.

Background:Aneurysmal subarachnoid hemorrhages are frequently complicated by hypertension and neurogenic myocardial stunning. Beta blockers may be used for management of these complications. We sought to investigate sympathetic nervous system modulation by beta blockers and their effect on radiographic vasospasm, delayed cerebral infarction, discharge destination and death.Methods:Retrospective chart review of 218 adults admitted to the ICU between 8/2004 and 9/2010 was performed. Groups were identified relevant to beta blockade: 77 were never beta blocked (No/No), 123 received post-admission beta blockers (No/Yes), and 18 were continued on their home beta blockers (Yes/Yes). Records were analyzed for baseline characteristics and the development of vasospasm, delayed cerebral infarction, discharge destination and death, expressed as adjusted odds ratio.Results:Of the 218 patients 145 patients developed vasospasm, 47 consequently infarcted, and 53 died or required care in a long-term facility. When compared to No/No patients, No/Yes patients had significantly increased vasospasm (OR 2.11 (1.06-4.16)). However, these patients also had significantly fewer deaths or need for long term care (OR 0.17 (0.05-0.64)), with decreased tendency for infarcts (OR 0.70 (0.32-1.55)). When compared to No/No patients, Yes/Yes patients demonstrated a trend toward increased vasospasm (OR 1.61 (0.50-5.29)) that led to infarction (OR 1.51 (0.44-5.13)), but with decreased mortality or need for long term care in a facility (OR 0.13 (0.01-1.30)).Conclusion:Post-admission beta blockade in aneurysmal subarachnoid hemorrhage patients was associated with increased incidence of vasospasm. However, despite the increased occurrence of vasospasm, beta blockers were associated with improved discharge characteristics and fewer deaths.

Citric Acid Cycle Metabolites Predict the Severity of Myocardial Stunning and Mortality in Newborn Pigs.

Myocardial infarction and chronic heart failure induce specific metabolic changes in the neonatal myocardium that are closely correlated to outcome. The aim of this study was to examine the metabolic responses to noninfarct heart failure and inotropic treatments in the newborn heart, which so far are undetermined. A total of 28 newborn pigs were instrumented with a microdialysis catheter in the right ventricle, and intercellular citric acid cycle intermediates and adenosine metabolite concentrations were determined at 20-minute intervals. Stunning was induced by 10 cycles of 3 minutes of ischemia, which was performed by occluding the right coronary artery, followed by 3 minutes of reperfusion. Animals were randomized for treatment with epinephrine + milrinone, dopamine + milrinone, dobutamine, or saline. University hospital animal laboratory. Ischemia-reperfusion induced right ventricular stunning and increased the concentrations of pyruvate lactate, succinate, malate, hypoxanthine, and xanthine (all, p < 0.01). During inotrope infusion, no differences in metabolite concentrations were detected between the treatment groups. In nonsurviving animals (n = 8), concentrations of succinate (p < 0.0001), malate (p = 0.009), and hypoxanthine (p = 0.04) increased compared with survivors, while contractility was significantly reduced (p = 0.03). Accumulation of citric acid cycle intermediates and adenosine metabolites reflects the presence of myocardial stunning and predicts mortality in acute noninfarct right ventricular heart failure in newborn pigs. This phenomenon occurs independently of the type of inotrope, suggesting that citric acid cycle intermediates represent potential markers of acute noninfarct heart failure.

Intradialytic Cardiac Magnetic Resonance Imaging to Assess Cardiovascular Responses in a Short-Term Trial of Hemodiafiltration and Hemodialysis.

Hemodynamic stress during hemodialysis (HD) results in recurrent segmental ischemic injury (myocardial stunning) that drives cumulative cardiac damage. We performed a fully comprehensive study of the cardiovascular effect of dialysis sessions using intradialytic cardiac magnetic resonance imaging (MRI) to examine the comparative acute effects of standard HD versus hemodiafiltration (HDF) in stable patients. We randomly allocated 12 patients on HD (ages 32-72 years old) to either HD or HDF. Patients were stabilized on a modality for 2 weeks before undergoing serial cardiac MRI assessment during dialysis. Patients then crossed over to the other modality and were rescanned after 2 weeks. Cardiac MRI measurements included cardiac index, stroke volume index, global and regional contractile function (myocardial strain), coronary artery flow, and myocardial perfusion. Patients had mean±SEM ultrafiltration rates of 3.8±2.9 ml/kg per hour during HD and 4.4±2.5 ml/kg per hour during HDF (P=0.29), and both modalities provided a similar degree of cooling. All measures of systolic contractile function fell during HD and HDF, with partial recovery after dialysis. All patients experienced some degree of segmental left ventricular dysfunction, with severity proportional to ultrafiltration rate and BP reduction. Myocardial perfusion decreased significantly during HD and HDF. Treatment modality did not influence any of the cardiovascular responses to dialysis. In conclusion, in this randomized, crossover study, there was no significant difference in the cardiovascular response to HDF or HD with cooled dialysate as assessed with intradialytic MRI.

Intensive Hemodialysis and Treatment Complications and Tolerability

Hemodialysis (HD) treatment can be difficult to tolerate. Common complications are intradialytic hypotension (IDH) and long time to recovery after an HD session. IDH, as defined by nadir systolic blood pressure <90mmHg and intradialytic decline > 30mmHg, occurs in almost 8% of HD sessions. IDH may be caused by aggressive ultrafiltration in response to interdialytic weight gain, can lead to myocardial stunning and cardiac arrhythmias, and is associated with increased risk for death. Long recovery time after a treatment session is also common. In DOPPS (Dialysis Outcomes and Practice Patterns Study), recovery time was 2 to 6 hours for 41% of HD patients and longer than 6 hours for 27%; recovery time was linearly associated with increased risks for death and hospitalization. Importantly, both decreases in blood pressure and feeling washed out or drained have been identified by patients as more important outcomes than death or hospitalization. Intensive HD likely reduces the likelihood of IDH. In the Frequent Hemodialysis Network trial, short daily and nocturnal schedules reduced the per-session probability of IDH by 20% and 68%, respectively, relative to 3 sessions per week. Due to lower ultrafiltration volume and/or rate, intensive HD may reduce intradialytic blood pressure variability. In a cross-sectional study, short daily and nocturnal schedules were associated with slower ultrafiltration and less dialysis-induced myocardial stunning than 3 sessions per week. In FREEDOM (Following Rehabilitation, Economics, and Everyday-Dialysis Outcome Measurements), a prospective cohort study of short daily HD, recovery time was reduced after 12 months from 8 hours to 1 hour, according to per-protocol analysis. Recovery time after nocturnal HD may be minutes. In conclusion, intensive HD can improve the tolerability of HD treatment by reducing the risk for IDH and decreasing recovery time after HD. These changes may improve the patient centeredness of end-stage renal disease care.

A case of reversible stress cardiomyopathy

Various physical and psychological insults can cause acute and rapidly reversible left ventricular dysfunction .This is called stress cardiomyopathy or Takotsubo cardiomyopathy. The act of Suicidal hanging involves intense physical stress and distressing emotional outburst. We report a case of rapidly reversible left ventricular dysfunction following attempted suicide by hanging. The pathogenesis of left ventricular dysfunction in hanging is multifactorial but the main mechanism is due to catecholamine surge causing myocardial stunning.

Limitation of Infarct Size and the Open Artery Hypothesis: A Conversation With Eugene Braunwald, MD.

Eugene Braunwald received an MD from the New York University School of Medicine. He completed an internal medicine residency at Johns Hopkins Hospital and cardiology fellowships at Mount Sinai Hospital, Columbia University, and the National Heart Institute. He served as chief of cardiology and subsequently clinical director of the institute. From 1968 to 1972, he was the founding chair of medicine at the University of California, San Diego. From 1972 to 1996, he served as chair of medicine at the Brigham and Women’s Hospital. In 1975, he was elected to the National Academy of Sciences. He is now the Distinguished Hersey Professor of Medicine at Harvard Medical School and a senior investigator of the TIMI Study Group, which he founded in 1984. Dr Braunwald replies: I became aware of the importance of AMI in 1951 during an elective in cardiology during my senior year at the New York University School of Medicine. At the time, AMI was by far the most common cause of death in adults in the United States. Of the patients who survived to be admitted to hospitals (no one knew how many AMI patients failed to reach hospital emergency departments), about one third died before discharge, either suddenly, presumably from an arrhythmia, or secondary to pump failure. Of the patients who were discharged alive, about one quarter died within a year, most frequently as a consequence of heart failure or recurrent MI. Pathologists had taught that AMI was usually associated with coronary thrombosis. Indeed, during my cardiology elective, Herrick’s classic article describing AMI was required reading. Its title, “Clinical Features of Sudden Obstruction of the Coronary Arteries,” showed how these 2 conditions (coronary occlusion and AMI) were intertwined.1 My direct involvement in the care of several patients who did not survive the acute event left …