Current Cardiology Reviews - Volume 4, Issue 1, 2008

Several primary trials report the adjunctive value of psychoeducational interventions for improving stable angina symptoms, health-related quality of life (HRQL) and psychological well-being; however, few high-quality metaanalyses have examined the overall effectiveness of these interventions. We used meta-analysis in order to determine the effectiveness of psychoeducational interventions for improving symptoms, HRQL and psychological well-being in stable angina patients. Seven trials, involving 949 participants total were included. Those who received psychoeducation experienced nearly 3 less angina episodes per week, delta (??)= -2.85, 95% CI, -4.04 to -1.66, and used sublingual (SL) nitrates approximately 4 times less per week, ??= -3.69, 95% CI -5.50 to -1.89, post-intervention (3-6 months). Significant HRQL improvements (Seattle Angina Questionnaire) were also found for physical limitation, ??= 8.00, 95% CI 4.23 to 11.77, and disease perception, ??= 4.46, 95% CI 0.15 to 8.77, but CIs were broad. A pooled estimate of effect on psychological wellbeing was not possible due to heterogeneity of measures. Psychoeducational interventions may significantly reduce angina frequency and decrease SL nitrate use in the short-term. These encouraging results must be interpreted with caution due to heterogeneity in methods and small samples. Larger, robust trials are needed to further determine the effectiveness of psychoeducation for stable angina management.

Long chain fatty acids (LCFAs) provide 70-80% of the energy for cardiac contractile activity. LCFAs are also essential for many other cellular functions, such as transcriptional regulation of proteins involved in lipid metabolism, modulation of intracellular signalling pathways, and as substrates for membrane constituents. When LCFA uptake exceeds the capacity for their cardiac utilization, the intracellular lipids accumulate and are thought to contribute to contractile dysfunction, arrhythmias, cardiac myocyte apoptosis and congestive heart failure. Moreover, increased cardiac myocyte triacylglycerol, diacylglycerol and ceramide depots are cardinal features associated with obesity and type 2 diabetes. In recent years considerable evidence has accumulated to suggest that, the rate of entry of long chain fatty acids (LCFAs) into the cardiac myocyte is a key factor contributing to a) regulating cardiac LCFA metabolism and b) lipotoxicity in the obese and diabetic heart. In the present review we i) examine the evidence indicating that LCFA transport into the heart involves a protein-mediated mechanism, ii) discuss the proteins involved in this process, including FAT/CD36, FABPpm and FATP1, iii) discuss the mechanisms involved in regulating LCFA transport by some of these proteins (including signaling pathways), as well as iv) the possible interactions of these proteins in regulating LCFA transport into the heart. In addition, v) we discuss how LCFA transport and transporters are altered in the obese/diabetic heart.

We are presenting a review of Isolated Systolic Hypertension (ISH) as a cardiovascular risk factor with emphasis on the perioperative period. Isolated systolic hypertension is associated with aging and is the most frequent subtype (65%) among patients with uncontrolled hypertension. ISH is strongly associated with increased risks of cardiac and cerebrovascular events exceeding those in comparably aged individuals with diastolic hypertension. Patients with ISH show an increase in left ventricular (LV) mass and an increase in the prevalence of left ventricular hypertrophy (LVH). These LV changes increase cardiovascular events and frequently lead to diastolic dysfunction (DD). Treatment to reduce elevated systolic blood pressure has been shown to reduce the risk of cardiovascular events. In the perioperative setting, essential hypertension has not been found to be a significant risk factor for cardiac complications. Most of the studies were based on the definition of essential hypertension and underpowered in sample size. The significance of perioperative ISH, however, is not well studied, partly due to its recognition only fairly recently as a cardiovascular risk factor in the non-surgical setting, and partly due to the evolving definition of ISH. Perioperative cardiac complications remain a significant problem to the healthcare system and to the patient. Although the incidence of perioperative cardiac complications is prominent in high-risk patients as defined by the Revised Cardiac Risk Index (RCRI), the bulk of the cardiac complications actually occur in low-risk group. Currently, little understanding exists on the occurrence of perioperative cardiac complications in low- risk patients. A factor such as ISH, with its known pathophysiological changes, is a potential perioperative risk factor. We believe ISH is an under-recognized perioperative risk factor and deserves further studying. Our research group has recently been funded by the Heart Stroke Foundation (HSF) to examine ISH as a perioperative risk factor (PROMISE Study).

Cardiogenic shock continues to be the most common cause of death in patients hospitalized with acute myocardial infarction. It has also been frequently associated with ST-segment elevation myocardial infarction (STEMI) and patients with co-morbidities. Cardiogenic shock presents with low systolic blood pressure and clinical signs of hypoperfusion. Rapid diagnosis and supportive therapy in the form of medications, airway support and intra-aortic balloon counterpulsation is required. Initial stabilization can be followed by reperfusion by fibrinolytic therapy, emergent percutaneous intervention (PCI) or coronary artery bypass grafting (CABG). The latter two have been found to decrease mortality in the long term. Research is being carried out on the role of inflammatory mediators in the clinical manifestation of cardiogenic shock. Mechanical support devices also show promise in the future.

Elucidating the underlying cause of unexplained syncope, palpitations or other possible arrhythmia-related symptoms is a formidable clinical challenge. Cardiac monitoring supplements the most important “test” in patients with syncope or palpitations, that of a thoughtful history and physical examination. Ideally, comprehensive physiologic monitoring during spontaneous symptoms would constitute what, at present, is an unattainable gold standard test for establishing a cause. Short of that goal, establishing an accurate symptom-rhythm correlation can often provide a diagnosis. Ambulatory outpatient monitoring is a powerful diagnostic tool for the evaluation of cardiac arrhythmias. Evolving technologies have provided a vast array of monitoring options for patients suspected of having cardiac arrhythmias, with each modality differing in duration of monitoring, quality of recording, convenience and invasiveness. Holter monitors, event monitors and external loop recorders are non-invasive and provide easily accessible short-term monitoring solutions. In instances where the diagnosis remains elusive, a more long-term strategy with an implantable loop recorder may be the preferred path.

The right ventricle (RV) is integral to normal cardiac function, but receives little attention in the medical literature. The etiologic causes of acute RV failure often differ from those encountered in left ventricular dysfunction. Thus, RV failure frequently requires diagnostic procedures and management strategies that differ from those routinely used in the management of intrinsic left ventricular dysfunction. In this summary, the structure and function of the RV will be reviewed, concentrating on the pathophysiologic mechanisms behind the development of RV dysfunction. We will then focus on two distinct populations of patients who are at risk for acute RV failure: those with chronic pulmonary arterial hypertension (PAH) and those with acute pulmonary embolism. In chronic PAH, we will examine clinical circumstances common to hospitalized patients that may provoke acute RV decompensation, as well as pharmacologic therapies that are unique to RV failure management in PAH. Individuals with acute RV failure in the setting of pulmonary embolism represent a group with particularly high mortality, and the specific diagnostic and management strategies that are important for improved survival will be discussed.

Leonardo da Vinci was born in Italy. Among the researchers and scientists, he is favourably known for his remarkable efforts in scientific work. His investigations of atherosclerosis judiciously combine three separate fields of research. In 1506, he finished his masterpiece, painting of Mona Lisa. A careful clinical examination of the famous painting reveals a yellow irregular leather-like spot at the inner end of the left upper eyelid and a soft bumpy well-defined swelling of the dorsum of the right hand beneath the index finger about 3 cm long. This is probably the first case of familial hypercholesterolemia (FH). The FH code of Leonardo da Vinci was given immense consideration by scientists like Carl Muller, who described the xanthomas tuberosum and angina pectoris. On the contrary, Akira Endo searched for microbial metabolites that would inhibit HMG-CoA reductase, the rate-limiting enzyme in the synthesis of cholesterol and finally, Michael Brown and Joseph Goldstein published a remarkable series of elegant and insightful papers in the 70s and 80s. They established that the cellular uptake of low-density lipoprotein (LDL) essentially requires the LDL receptor. In conclusion: this was the real Code of Leonardo da Vinci.

A 48-hour course of intravenous unfractionated heparin (UFH) is the standard of treatment in conjunction with fibrin-specific thrombolysis in ST-elevation myocardial infarction (STEMI). In recent trials, the efficacy and safety of inhospital administration of subcutaneous low-molecular-weight heparins (LMWH), previously proven effective in non-STelevation acute coronary syndromes, have been investigated in the setting of STEMI. The aim of this review was to evaluate the available evidence supporting the use of LMWH in STEMI. Overall, about 27,000 patients treated with various thrombolytic regimens, were included in 12 open-label randomized clinical trials, where dalteparin, reviparin or enoxaparin were administered. While acknowledging the wide variability in study dimensions, designs and end-points, a higher efficacy of LMWH was observed overall as compared to placebo, and also to UFH (mainly as regards the occurrence of reinfarction). As regards safety, bleedings were more frequent than placebo and comparable to UFH in LMWH groups, with the exception of the pre-hospital ASSENT-3 PLUS trial, where in elderly patients, enoxaparin had an incidence of intracranial hemorrhage twice higher than UFH. In a recent double-blind, randomized, mega-trial including over 20,000 patients, the superior efficacy on in-hospital and 30-day adverse cardiac events (namely reinfarction), and comparable safety on intracranial bleedings, of enoxaparin compared to UFH, was shown. In conclusion, in-hospital subcutaneous administration of dalteparin, reviparin and enoxaparin, as an adjunct to various thrombolytics in STEMI, appears feasible and at least as effective and safe as 48-hour intravenous treatment with UFH. In accordance with the available strongest evidence, an initial intravenous bolus of enoxaparin followed by twice daily subcutaneous administration for about 1 week should be the preferred regimen, and should be strongly considered instead of intravenous UFH. Along with its easiness of use, not requiring laboratory monitoring, subcutaneous administration of LMWH following STEMI treated with thrombolysis allows extended antithrombotic treatment, while permitting early mobilization (and rehabilitation) of patients.