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Programmed ventricular stimulation in patients with left ventricular dysfunction and ventricular tachycardia: effects of acute hemodynamic improvement due to nitroprusside.

To assess the electrophysiologic effects of acute hemodynamic improvement in patients with left ventricular systolic dysfunction, 12 patients with a left ventricular ejection fraction less than 0.40 and a history of sustained monomorphic ventricular tachycardia were studied. All patients had underlying coronary artery disease. Patients underwent programmed cardiac stimulation in random order during a baseline period and with nitroprusside infusion. Mean pulmonary capillary wedge pressure decreased from 20 +/- 8 mm Hg at baseline study to 8 +/- 3 mm Hg during nitroprusside infusion (p less than 0.0001). Pulmonary artery, right atrial and systemic arterial pressures also decreased with nitroprusside (p less than 0.01). Cardiac output did not change. Left ventricular dimensions, determined by two-dimensional echocardiography, decreased significantly during nitroprusside infusion. The right ventricular effective refractory period, measured during ventricular drive trains at cycle lengths of 400 and 600 ms, were similar during baseline and nitroprusside periods (271 +/- 30 versus 274 +/- 31 ms at 600 ms, and 249 +/- 25 versus 246 +/- 18 ms at 400 ms). In 2 patients no ventricular arrhythmias were induced during either study period; in the other 10, ventricular tachyarrhythmias were induced during both periods. The mean number of extrastimuli required to induce a ventricular tachyarrhythmia was similar during the baseline period (1.8 +/- 0.6) and during nitroprusside infusion (1.9 +/- 0.7). As well, the mean cycle length of ventricular tachycardia induced was similar during the baseline period (347 +/- 61 ms) and during nitroprusside infusion (342 +/- 70 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Impact of implantable defibrillators and resynchronization therapy on outcome in patients with left ventricular dysfunction--a meta-analysis.

BACKGROUND: The clinical benefits of cardiac resynchronization therapy (CRT) and primary prophylactic implantable cardioverter defibrillator (ICD) in patients with left ventricular systolic dysfunction (LVSD) are debated. OBJECTIVE: To evaluate by a meta-analysis the effect of CRT and prophylactic ICD therapy in patients with LVSD. METHODS: Eligible trials evaluating the effect of CRT vs. no-CRT, ICD vs. no-ICD and adding ICD to CRT vs. no-ICD were selected and meta-analyzed. The outcomes were: all cause mortality, cardiac mortality, hospitalization for heart failure and change in exercise tolerance and New York Heart Association class. RESULTS: Implantation of CRT reduced all cause mortality odds ratio (OR) = 0.73 (0.60-0.89) p = 0.002 and hospitalization for heart failure OR = 0.60 (0.45, 0.80) p = 0.001, increased peak oxygen consumption by 1.77 (0.32-3.22) ml/kg/min p = 0.017 and improved New York Heart Association class by at least one class with OR = 1.52 (1.30, 1.77) p < 0.0001. Implantation of ICD reduced all-cause mortality OR = 0.75 (0.59-0.96) p = 0.025 and cardiac mortality OR = 0.63 (0.48, 0.82) p = 0.001. Adding ICD to CRT reduced all cause mortality OR = 0.69 (0.53-0.91) p = 0.008. CONCLUSION: Selective patients with LVSD benefit from CRT, ICD or both. Further investigations are necessary to clarify which patients benefit most from a single or combined device implantation.

Defibrillators, Implantable↗

Role of heart rate reduction in the treatment of exercise-induced myocardial ischaemia.

The role of bradycardia in reducing exercise-induced ischaemia and wall dysfunction was examined in dogs with single vessel chronic coronary artery stenosis created using an ameroid constrictor. Treadmill exercise produced significant regional myocardial ischaemia (blood flow measured using microspheres) and contractile dysfunction (systolic wall thickening measured with sonomicrometers). Dogs were initially studied during a control run before and during a second identical run after administration of the cardioselective beta-adrenergic blocker atenolol, which improved regional ischaemic function from 4.4 +/- 3.7% to 8.5 +/- 2.8% and subendocardial perfusion from 0.43 +/- 0.23 to 0.55 +/- 0.29 ml min-1 g-1. In another group of dogs during a run with atenolol, the heart rate was paced to match the rate observed in the control run. During the atenolol run with pacing, all beneficial effects of atenolol observed at the reduced exercise heart rate were lost. A third group of dogs received the bradycardic agent UL-FS 49 (1.0 mg kg-1, i.v.) prior to exercise. UL-FS 49 produced a heart rate reduction during exercise from 230 +/- 19 to 139 +/- 10 beats min-1; this was associated with an increase in systolic wall thickening from 9.3 +/- 5.0% (during the control run) to 21.5 +/- 8.4%, thereby eliminating the exercise-induced contractile dysfunction. Transmural myocardial blood flow per beat to the poststenotic myocardium was improved significantly from 4.8 X 10(-3) +/- 1.9 X 10(-3) ml beat-1 to 9.8 X 10(-3) +/- 1.7 X 10(-3). Atrial pacing to match heart rate to the control exercise rate during the UL-FS 49 run did not eliminate all of the improvement in systolic wall thickening.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Postcardioplegia acute cardiac dysfunction and reperfusion injury.

In cardiac surgery, an obligatory period of ischemia is imposed in order to provide a convenient operative field. Brief periods of ischemia produce systolic and diastolic abnormalities related to pathology occurring during ischemia per se (ischemic injury) or expressed after the onset of reperfusion (reperfusion injury). In the surgical setting, ischemia may be encountered preoperatively with preexisting coronary disease, hypotension, or ventricular fibrillation, between intermittent infusions of cardioplegia solutions, or as a result of maldistribution of cardioplegia solution. The potential for reperfusion injury exists not only at the time of cross-clamp removal, but also with each infusion of cardioplegia solution. Infusion of cardioplegic solution is, in fact, a form of reperfusion to previously ischemic myocardium. Ischemic injury and reperfusion injury are intimately linked in that the severity of ischemia sets the stage for and determines, in part, the extent of reperfusion injury. Mild-to-moderate systolic dysfunction, which may be called "postcardioplegia stunning," remains a significant complication after cardiac surgery. More significant postoperative functional depression may occur in hearts with severe preoperative dysfunction, and in operations requiring long cross-clamp times. In addition, the failure to adequately distribute cardioplegic solution to all areas of the myocardium because of coronary stenoses, high coronary resistance or inadequate delivery pressure-flow relations, contributes to postcardioplegia dysfunction. However, the cardioplegic solution itself may also contribute to postcardioplegic dysfunction by creating temporary ionic and metabolic abnormalities. In addition, systemic hypocalcemia or hyperkalemia resulting from using large doses of cardioplegic solution may temporarily aggravate postcardioplegic mechanical dysfunction. Current formulations and strategies for delivery of cardioplegia solutions are designed to address the various contributors to both ischemic and reperfusion injury that may impact on postoperative mechanical performance. Ischemic injury is avoided by reducing myocardial oxygen demand by engaging immediate arrest and cooling the heart to approximately 10 degrees centigrade, and intermittently infusing solution to reoxygenate the myocardium, maintain hypothermia, and wash out accumulated metabolites. Reperfusion injury may be avoided by infusing hyperosmotic solutions at moderate pressures, and by incorporating oxygen radical scavengers or inhibitors to reduce membrane lipid peroxidation, myocellular and microcirculatory (endothelium) damage.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Predictors of left ventricular dysfunction in patients with Takayasu's or giant cell aortitis.

OBJECTIVES: The aim of this study was to determine the clinical and angiographic predictors of left ventricular systolic dysfunction (LVSD) from a relatively large and angiographically characterized Takayasu's or Giant Cell aortitis (TA/GCA) population. BACKGROUND: LVSD in patients with TA/GCA has been described in case reports and attributed variously to hemodynamic and immunologic factors. The predictors of LVSD in patients with angiographically confirmed TA/GCA are not known. METHODS: We identified 78 patients with angiographically confirmed TA/ GCA that underwent transthoracic echocardiography (TTE) at Mayo Clinic. Echocardiograms were then reviewed independently by reviewers blinded to clinical and angiographic data. LVSD was defined as an ejection fraction (LVEF) less than 50%. RESULTS: The study population was 84% Caucasian (54/78), 91% female (58/78), and had a mean age of disease onset of 30 years (+/- 15 years). LVSD was present in 14 of 78 patients (18%) with TA/GCA. The mean LVEF in the LVSD group (n = 14) was 37% +/- 7%, compared to an LVEF of 62% +/- 6% (p < 0.0001) in those without LVSD (n = 64). LVSD was not associated with hypertension or aortic regurgitation (p > 0.5). However, LVSD was found in 43% (9/21) of patients with aortic arch involvement, versus only 9% (5/57) of patients without aortic arch involvement (p = 0.0013). Patients with LVSD had a median of 2 (range 1-4) involved aortic segments compared to a median of 1 (range 1-4) among those without LVSD (p = 0.013). CONCLUSIONS: In TA/GCA aortitis, LVSD is associated with involvement of the aortic arch and with the greater extent of aortic involvement. The hemodynamic variables, aortic regurgitation and systemic hypertension, were not associated with LVSD, consistent with reports that cardiac inflammation is responsible for LVSD in a majority of cases. Ours is the first study to estimate an incidence of LVSD in patients with TA/GCA aortitis, which was 18%.

Adult↗

Tei index as a method of evaluating left ventricular diastolic dysfunction in acute myocardial infarction.

INTRODUCTION: The Doppler index of overall left ventricular (LV) myocardial performance--the Tei index--has been shown to be a reliable indicator of all changes in LV systolic dysfunction, retaining an inverse relationship with the ejection fraction. The aim of this study was to examine the corresponding behaviour in relation to LV diastolic dysfunction in patients with acute myocardial infarction (AMI), a relationship that has not been studied previously. METHODS: The study included 105 patients (77 men) with first AMI who were classified into four groups according to the severity of LV diastolic dysfunction: a) 25 patients with normal diastolic function (NDF), b) 36 with decreased peak filling rate pattern (DFR), c) 33 with impaired relaxation (IR) and d) 11 with pseudonormal or restrictive physiology (PN/RP). A complete echocardiographic study, including all conventional systolic and diastolic echo/Doppler parameters as well as measurement of the Tei index, was performed on the eighth post-infarction day (mean 8.07 +/- 0.96 days) in all patients. RESULTS: In the patients with IR (0.77 +/- 0.05) the index was significantly greater than in those of the NDF (0.55 +/- 0.03, p<0.01) or DFR (0.65 +/- 0.02, p<0.01) groups. The index in the DFR group was greater than in the NDF group, though not significantly so. In contrast, the index in the PN/RP patients (0.59 +/- 0.05) was significantly lower than in the patients with IR (p<0.01), whereas it did not differ from that of the patients in the NDF or DFR groups ("pseudonormalisation" of the index). CONCLUSIONS: The Tei index detects with reliability milder types of diastolic dysfunction. However, because of its "pseudonormalisation" in patients with PN/RP, the Tei index cannot be considered a reliable indicator of more severe patterns of LV diastolic dysfunction in AMI patients.

Aged↗

Current Treatment Options for CHF Management: Focus on the Renin-Angiotensin-Aldosterone System.

Heart failure (HF) is highly prevalent in our society and its incidence is increasing in concert with the growing aged population. Experimental and clinical studies have consistently shown that HF is ameliorated by inhibition of the renin-angiotensin-aldosterone system (RAAS). Acknowledging that heightened activation of the RAAS contributes significantly to HF progression has led to the development of pharmacologic antagonists of RAAS components that have greatly improved both symptoms and prognosis of patients suffering from this syndrome. Angiotensin-converting enzyme (ACE) inhibitors represent the first developed agents that block the production of angiotensin II, and have been shown to be effective across a broad spectrum of patients with HF, including those with asymptomatic left ventricular dysfunction to overt HF. Initiation of ACE inhibitors prior to the onset of symptoms in those with left ventricular systolic dysfunction, and as early as feasible following a myocardial infarction, has been shown to reduce mortality and the development of overt HF in several clinical trials. Clinical data also support the use of angiotensin II receptor antagonists as an alternative to ACE inhibitors in patients who are allergic to, or intolerant of, ACE inhibitors. Agents that antagonize aldosterone via blockade of mineralocorticoid receptors improve clinical outcomes in patients with advanced HF or those with reduced ejection fraction and HF following an acute myocardial infarction. Maximally inhibiting the RAAS, in conjunction with other neurohormonal systems (eg, the sympathetic nervous system by b-adrenergic blockade), leads to improved clinical outcomes in HF, a highly prevalent and costly disease in our society.

Journal Article↗

Diastolic heart failure: recognition, diagnosis and management.

A variety of community-based epidemiological studies have suggested that 30-50% of patients with heart failure symptoms appear to have preserved left ventricular (LV) systolic function when assessed by echocardiography or similar techniques suggesting 'diastolic heart failure' (DHF) as its cause. The prognosis of these patients is characterised by morbidity and mortality similar to, but less overt than, patients with systolic dysfunction. However, rates of readmission for symptom control are broadly similar in patients with DHF or in those with systolic impairment. Thus, there are many similarities in the portrayal of both systolic and DHF but equally; there are also many key differences. Certainly, while there are several successful therapies for patients with systolic heart failure, the management of patients with DHF is poorly defined. In this review, the gaps in current knowledge and practice, which is creating this therapeutic void will be addressed.

Anti-Arrhythmia Agents↗

[Neoton and thrombolytic therapy of myocardial infarction].

AIM: To evaluate neoton therapy effects in acute myocardial infarction (MI) on systolic function of the left ventricle, arrhythmia and clinical symptoms in patients on thrombolytic therapy (TLT). MATERIAL AND METHODS: 106 males with Q-MI entered the study. 47 received treatment without TLT and neoton, 30 patients received TLT with streptokinase preparations, 29 patients were given streptokinase preparations and neoton. Left ventricular systolic function was measured by echocardiography on day 1, 3, 7, 14, 21 and 28; arrhythmia was analysed at Holter monitoring in day 1 and 2 of MI. RESULTS: TLT failed to arrest progression of left ventricular dilation by the end of the hospital stay. Patients given neoton in acute period of MI had no increase in the end systolic and diastolic volumes of the left ventricle in the course of the first months after MI onset. Antiarrhythmic action of neoton manifested on MI day 2. CONCLUSION: Neoton given to MI patients receiving TLT prevents progression of left ventricular systolic dysfunction and establishment of predictors of unfavourable outcome.

Adult↗

Plasma atrial natriuretic peptide and brain natriuretic peptide are increased in septic shock: impact of interleukin-6 and sepsis-associated left ventricular dysfunction.

OBJECTIVE: Interest has recently focused on the use of neurohormonal markers such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) as indices of left ventricular systolic dysfunction and prognosis in heart failure. Also, peptides belonging to the interleukin-6 (IL-6) family have been shown to induce ANP and BNP secretion. We hypothesized that BNP and ANP spillover in the peripheral circulation reflects left ventricular dysfunction and IL-6 production in septic shock. DESIGN AND SETTING: Retrospective, clinical study in the medical intensive care unit of a university hospital. PATIENTS AND PARTICIPANTS: 17 patients with septic shock and 19 control subjects. INTERVENTIONS: Collection of clinical and demographic data in relation to ANP, BNP, IL-6, and soluble TNF receptors (sTNF-R-p55, sTNF-R-p75) in plasma over a period of 4 days. MEASUREMENTS AND RESULTS: In septic shock we found a significant increase in ANP (82.7+/-9.9 vs. 14.9+/-1.2 pg/ml) and BNP (12.4+/-3.6 vs. 5.5+/-0.7 pg/ml). Plasma ANP peaked together with IL-6. Peaks of ANP and IL-6 were significantly correlated (r=0.73; p<0.01). BNP was inversely correlated to cardiac index (r=-0.56; p<0.05). CONCLUSIONS: ANP and BNP increase significantly in patients with septic shock. BNP reflects left ventricular dysfunction. ANP is related to IL-6 production rather than to cardiovascular dysfunction.

Atrial Natriuretic Factor↗

Clinical utility of tissue Doppler imaging in prediction of atrial fibrillation after coronary artery bypass grafting.

BACKGROUND: Atrial systolic dysfunction in patients with coronary artery disease might influence the development of atrial fibrillation after coronary artery bypass grafting (CABG). Tissue Doppler imaging of the mitral annulus during atrial systole has proved to quantify, accurately, left atrial contractile function. Therefore, the aim of the present study was to investigate the correlation between preoperative left atrial dysfunction assessed by tissue Doppler and postoperative atrial fibrillation after CABG. METHODS: We studied a total of 96 patients (mean age 67 +/- 6 years; range, 55 to 81) undergoing CABG who were preoperatively in sinus rhythm. All patients underwent a preoperative transthoracic echocardiography with tissue Doppler evaluation. Until the day of discharge, all patients were monitored with continuous electrocardiographic telemetry. RESULTS: There were no hospital deaths. Postoperative atrial fibrillation was recorded in 24 of 96 patients (25%). Patients with postoperative atrial fibrillation were significantly older (70 +/- 6 vs 65 +/- 8 years; p = 0.006), had a preoperative larger left atrium diameter (38 +/- 5 vs 36 +/- 4 mm; p = 0.045), a larger left atrium area (13.2 +/- 3.4 vs 11.5 +/- 2.3 cm2; p = 0.007), and a lower peak atrial systolic mitral annular tissue Doppler velocity (10 +/- 3 vs 13 +/- 5 cm/second; p = 0.01). Stepwise logistic regression analysis showed that age 70 years or greater (p = 0.02; odds ratio [OR] 2.0), preoperative medication with beta-blockers (p = 0.04; OR 0.7), left atrium area 13 cm2 or greater (p = 0.02; OR 2.5), and peak atrial systolic mitral annular tissue Doppler velocity 9 cm/second or less (p = 0.03; OR 1.8) were independently related with the incidence of postoperative atrial fibrillation. CONCLUSIONS: Tissue Doppler is useful for assessing preoperative atrial dysfunction and predicting atrial fibrillation after CABG. Further studies are needed to confirm this finding.

Aged↗

Assessment of left ventricular systolic function in patients with idiopathic mitral valve prolapse using dobutamine stress echocardiography.

BACKGROUND: Some previous studies performed with radionuclide ventriculography and thallium scintigraphy reported that patients with idiopathic mitral valve prolapse (MVP) had some degree of left ventricular (LV) systolic dysfunction and that this dysfunction was more commonly found in symptomatic patients. HYPOTHESIS: The aim of the present prospective study was to investigate LV systolic function and its relationship with symptoms in patients with MVP with dobutamine stress test without associated certain mitral regurgitation and coronary artery disease. METHODS: Thirty-three patients with echocardiographically diagnosed idiopathic MVP were enrolled into the study and were divided into two groups as symptomatic (MVP-s) and asymptomatic (MVP-a). Patients underwent dobutamine stress echocardiography (DSE) to determine wall motion abnormalities and ejection fraction (EF) changes during rest state and increased heart rates. Results were compared with the DSE findings of 25 healthy individuals. RESULTS: Symptomatic patients (MVP-s) had lower EFs during the pretest period than the control group (59.0 +/- 4.8% and 68.3 +/- 5.7%, respectively, p < 0.05). Basal wall motion abnormalities were found in one patient in the MVP-a group (6%) and in two patients in the MVP-s group (12%). During DSE, new wall motion abnormalities (inferoapical dyskinesia) occurred in two patients in the MVP-s group at submaximal heart rates. For EF values calculated when patients reached submaximal heart rate, the MVP-s group showed only a 2.7 +/- 3.1% increase from baseline values. This increase was 5.1 +/- 3.8% in the MVP-a group and 9.3 +/- 4.3% in the control group (p < 0.05 between MVP-s and control groups). CONCLUSION: There is a close relationship between symptoms and ventricular function in patients with idiopathic MVP, and although many asymptomatic patients had nearly normal LV function, a subgroup of symptomatic patients showed diminished LV function and wall motion abnormalities.

Adult↗

Diastolic heart failure: a myth.

PURPOSE OF REVIEW: Until recently, patients with heart failure and preserved ejection fraction (HFprEF) have been excluded from nearly all large clinical trials in heart failure. Based on the conjecture that this clinical picture of heart failure, also known as diastolic heart failure, may be different from other forms of heart failure, several recent and ongoing clinical trials have targeted more specifically this patient population. The present review critically re-evaluates the pathophysiological rationale for such trials. RECENT FINDINGS: Novel techniques to evaluate cardiac performance have revealed that HFprEF is a consequence of significant systolic dysfunction of the ventricular muscular pump in the presence of a preserved performance of the ventricular hemodynamic pump. Diastolic and systolic heart failure are the mere extremes of a spectrum of different phenotypes of one and the same disease. Ongoing research explores the various disease modifiers, or protective pathways, that delay the progression of remodeling in patients with HFprEF. Although, currently, therapy to improve the prognosis of HFprEF is essentially the same as for other forms of heart failure, the latter ongoing studies may help, in addition, in developing novel and more patient-specific therapeutic strategies in these patients. SUMMARY: HFprEF constitutes a heterogenous group of different phenotypes within one continuous spectrum reflecting heart failure as one disease entity. No pathophysiological basis currently warrants setting up empirical clinical trials based on an arbitrary subdivision of patients with heart failure.

Cardiac Output, Low↗

Evaluation of asymptomatic patients with chronic Chagas disease through ambulatory electrocardiogram, echocardiogram and B-Type natriuretic peptide analyses.

OBJECTIVE: To evaluate asymptomatic patients with chronic Chagas disease to determine prevalence of ventricular arrhythmias, left ventricular dysfunction, and B-type natriuretic peptide (BNP) plasma levels. METHODS: One hundred and six patients from the Chagas disease outpatient clinic underwent clinical evaluation, electrocardiogram (ECG), cardiothoracic index (CTI), ambulatory electrocardiogram (Holter monitoring), echocardiogram, and BNP measurement and then were distributed into three groups: GI, with normal ECG (n = 50); GIIA, with ECG changes characteristic of Chagas disease (n = 31); and GIIB, with other ECG changes (n = 25). RESULTS: The most common electrocardiographic changes were the following. GIIA: complete right bundle branch block (35%), left anterior hemiblock (35%), and electrically inactive areas (32%); GIIB: inferolateral repolarization change (28%), and left ventricular overload (24%). Mean CTI index values were similar (p = 0.383). Ventricular arrhythmia prevalence was higher in the GIIA (77%) and GIIB (75%) groups than in the GI group (46%) (p = 0.002). Ventricular dysfunction was more prevalent in the GIIA (52%) and GIIB (32%) groups than in the GI group (14%) (p = 0.001). Systolic dysfunction was more prevalent in the GIIA group (29%) than in the GIIB (20%) and GI groups (2%) (p < 0.001). Diastolic dysfunction was more prevalent in the GIIA (42%) and GIIB (28%) groups than in the GI group (12%) (p = 0.005). Mean B-type natriuretic peptide levels were 30 +/- 88 pg/mL in the GI group, 66 +/- 194 in the GIIA group and 24 +/- 82 for the GIIB group (p = 0.121), respectively. CONCLUSION: Arrhythmias and left ventricular dysfunction are more prevalent in asymptomatic patients with chronic Chagas disease and abnormal ECG than in patients with normal ECG. Plasma BNP levels were similar among the groups.

Adult↗

[National and international guidelines ignore significant cause of heart failure. Diastolic dysfunction is often the cause of heart failure in the elderly and in women].

Comparison of patients treated for chronic heart failure at a large hospital with patients included in major treatment studies published during the past ten years yielded important information. The former series was characterised by greater proportions of the elderly and of women than were the series recruited to the often cited ACE (angiotensin-converting enzyme) inhibitor studies. Although only patients with systolic dysfunction were recruited to the latter studies, a substantial body of evidence suggests the prevalence of severe heart failure among patients with normal systolic function to increase with increasing age. Thus, as many as 50 per cent of all elderly patients with chronic heart failure may have normal systolic function. In most cases, the heart failure is probably due to diastolic dysfunction, a condition that still lacks both a simple diagnostic procedure and a well-documented treatment.

Aged↗

Effects of sodium nitroprusside in aortic stenosis associated with severe heart failure: pressure-volume loop analysis using a numerical model.

In the recently published clinical study [Use of Nitroprusside in Left Ventricular Dysfunction and Obstructive Aortic Valve Disease (UNLOAD)], sodium nitroprusside (SNP) improved cardiac function in patients with severe aortic stenosis (AS) and left ventricular (LV) systolic dysfunction. We explored the possible mechanisms of these findings using a series of numerical simulations. A closed-loop lumped parameters model that consists of 24 differential equations relating pressure and flow throughout the circulation was used to analyze the effects of varying hemodynamic conditions in AS. Hemodynamic data from UNLOAD study subjects were used to construct the initial simulation. Systemic vascular resistance (SVR), heart rate, and aortic valve area were directly entered into the model while end-systolic and end-diastolic pressure-volume (P-V) relationships were adjusted using previously published data to match modeled and observed end-systolic and end-diastolic pressures and volumes. Initial simulation of SNP treatment by a reduction of SVR was not adequate. To obtain realistic model hemodynamics that reliably reproduce SNP treatment effects, we performed a series of simulations while simultaneously changing end-systolic elastance (E(es)), end-systolic volume at zero pressure (V(0)), and diastolic P-V shift. Our data indicate that either an E(es) increase or V(0) decrease is necessary to obtain realistic model hemodynamics. In five patients, we corroborated our findings by using the model to duplicate individual P-V loops obtained before and during SNP treatment. In conclusion, using a numerical model, we identified ventricular function parameters that are responsible for improved hemodynamics during SNP infusion in AS with LV dysfunction.

Aortic Valve Stenosis↗

Asymptomatic valvular disease: who benefits from surgery?

Routine physical examination and noninvasive imaging frequently lead to the diagnosis of valvular heart disease in asymptomatic patients. The decision to proceed to surgical repair or replacement is based on an informed evaluation of the risks of surgery versus those encountered with a nonoperative course. In determining whether symptoms are present, stress testing may be helpful, as many patients with significant valvular lesions have a tendency to limit their daily physical exertion to levels that do not provoke symptoms. The two most feared consequences of conservative management, sudden death and permanent myocardial damage, are rare in asymptomatic patients with severe aortic stenosis or regurgitation. Surgery for asymptomatic aortic stenosis is performed only for certain high-risk subsets of patients, including those with left ventricular dysfunction, ventricular arrhythmia, and critically small valves. Asymptomatic patients with aortic regurgitation and mitral regurgitation should undergo surgery if they have systolic dysfunction or marked ventricular enlargement.

Adult↗

Do the presence and amount of dysfunctional but viable myocardium affect the perioperative outcome of coronary artery bypass graft surgery?

The aim of our study was to assess the influence of the presence and amount of dysfunctional but viable myocardium on the perioperative outcomes in patients with coronary artery disease and moderate-to-severe left ventricular systolic dysfunction, who underwent coronary artery bypass graft surgery. Viability evaluation with low-dose dobutamine echocardiography was performed in 302 consecutive patients with coronary artery disease and left ventricular ejection fraction < or =40%, who were referred for coronary angiography and potential coronary revascularization. To quantify the amount of dysfunctional but viable myocardium, wall motion was scored using a 16-segment model. The dysfunctional segments were defined as viable if they exhibited improvement in their thickening by at least one grade. One hundred and twenty-seven patients underwent coronary artery bypass graft surgery. The perioperative outcomes were evaluated in 122 of them. Five patients were excluded because of inability to revascularize all vessels supplying dysfunctional but viable myocardial segments. Twenty-five patients exhibited a large amount of dysfunctional but viable myocardium (> or =6 segments, group A), 59 patients had a small amount of such myocardium (2-5 segments, group B), and 38 patients were found to have their dysfunctional myocardium irreversibly damaged (group C). The perioperative mortality in groups A, B, and C was 4, 10, and 11% (all P = NS), respectively. The rate of perioperative Q-wave myocardial infarction was 8, 10, and 3% (all P = NS), respectively. Similarly, there were no significant differences among the groups with respect to perioperative outcome variables including ventricular arrhythmias, duration and magnitude of catecholamine support, renal failure, pulmonary edema, and need for mechanical ventricular support or artificial ventilation. In patients with coronary artery disease and moderate-to-severe left ventricular dysfunction who underwent coronary artery bypass graft surgery, the presence and amount of dysfunctional but viable myocardium did not influence the perioperative outcome.

Adult↗