heart

Chronic heart failure has been extensively characterized as a disorder arising from a complex interaction between impaired ventricular performance and neurohormonal activation. Since beta adrenoceptor blocking agents are currently considered an integral component of therapy for the management of patients with severe chronic heart failure; several well designed clinical trials have been conducted to determine the morbidity and mortality benefits of these agents these studies, however did not yield the same results in terms of morbidity and mortality benefits. Currently only Bisoprolol, Carvedilol and sustained release metoprolol succinate have clinically proven and convincing morbidity and mortality benefits the current list of approved medicines of the National Health Insurance Scheme (NHIS) of the republic of Ghana does not provide coverage for these lifesaving therapeutic agents. The objective of this review was to collate the relevant scientific evidence that will convince the authorities at the National Health Insurance Authority (NHIA) of the Republic of Ghana to include at least one of the evidence based beta adrenoceptor blocking agents in the list of approved medicines. A thorough search on the internet was conducted using Google scholar to obtain only the clinically relevant studies associated with the benefits of beta adrenoceptor blocking agents in patients with chronic heart failure published in the English language. The phrases beta adrenoceptor blocking agents and chronic heart failure were used as search engines. The search engine yielded several studies that met the predefined inclusion criteria. However, only the Cardiac Insufficiency BIsoprolol Studies (CIBIS-I and CIBIS-II), Carvedilol Prospective Randomized Cumulative Survival Study (COPERNICUS) and Metoprolol CR/XL Randomized Intervention Trial (MERIF-HF) because of the clinical relevance of their findings Beta adrenoceptor blocking agents such as atenolol and propranolol have been used in the management of patients with chronic heart failure. However, their efficacy and optimal dose in reducing mortality have not been scientifically established not all beta adrenoceptor blocking agents scientifically studied provide the same degree of clinically meaningful and convincing morbidity and mortality benefits in patients with chronic heart failure.

Background: Contrast-induced acute kidney injury (CI-AKI) is an important cause of increasing the hospital stay and in-hospital mortality. By increasing intra-renal vasoconstriction, left ventricular ejection fraction (LVEF) can increase the risk of CI-AKI. We sought to investigate whether LVEF can impact the incidence of CI-AKI after cardiac catheterization and whether it can be used to predict CI-AKI. Methods: Patients underwent cardiac catheterization from December 2017 to February 2018 at Jersey Shore University Medical Center were enrolled in the study. Contrast-induced acute kidney injury (CI-AKI) was defined as an increase in serum creatinine of ≥ 0.5 mg/dL or an increase of ≥ 25% from the pre-procedure value within 72 hours post-procedure. The maximum allowable contrast dose was calculated using the following formula: (5* (weight (kg)/creatinine level (mg/dL)). A multivariable logistic regression analyses, controlling for potential confounders, were used to test associations between LVEF and CI-AKI. Results: 9.6% had post catheterization CI-AKI. A total of 18 out of 44 (44%) of patients who had CI-AKI also had ongoing congestive heart failure. No statistically significant association found neither with maximum allowable contrast (p = 0.009) nor ejection fraction (p = 0.099) with the development of CI-AKI. Conclusion: In spite of the fact that no statistically significant relationship found between the percentage maximum contrast dose and the ejection fraction with the post-procedure CI-AKI, we heighten the essential of employing Maximum Allowable Contrast Dose (MACD) and ejection fraction in patients undergoing PCI to be used as a clinical guide to predict CI-AKI.

A key platform underpinning the traditional understanding of the cardiovascular system, with respect to the behavior of large arterial vessels, is Otto Frank’s Windkessel Hypothesis [1]. This hypothesis posits simply that the smooth muscle walls of large arteries do not undergo rhythmic contractions in synchrony with the heartbeat but, rather, behave as passive elastic tubes undergoing distension from pulsatile pressure waves. The Windkessel Hypothesis is elegant, well described for over a century, ingrained in the understanding of cardiovascular medicine and physiology, and simply wrong. Several groups have now shown that the arterial smooth muscle wall undergoes rhythmic activation in synchrony with the heartbeat in a variety of tissues, including human brachial artery; canine coronary, femoral, and carotid arteries; rabbit aorta; feline pulmonary artery and rodent aorta [2-8]. The phasing of these events is such that the upstroke of the contraction slightly precedes the upstroke of the pulse wave, suggesting nomenclature for the events as pulse synchronized contractions, or PSCs [3,6-8]. PSCs have been found to be of neurogenic origin, sensitive to the neural blocker tetrodotoxin [3,8]. Although the specific neural pathways regulating PSCs have not been elucidated, the alpha-adrenergic system is at least partially involved, as evidenced by reduction or blockade of PSCs by the alpha-adrenergic blocker phentolamine [8]. Further, PSCs have not been observed following vessel excision in in vitro studies, as an intact nervous system is not present. The pacemaker for the PSC resides in the right atrium, as suggested by two lines of evidence. First, pacing of the right atrial region to faster than spontaneous frequencies leads to a one-to-one correspondence of PSC frequency with the stimulation rate [3]. Additionally, excision of the right, but not the left, atrial appendage results in elimination of PSCs [3]. As the pacemaker region for PSCs and the heartbeat both lie in the right atrium, this may potentially allow for coordination between the heartbeat and pulse wave with PSCs [3,5,8]. Extensive evaluations also have been performed showing the PSC was not an artifact produced either by cardiac contractility or from the vessel distension from the pulse wave [3,5,6].

Purpose: This was a prospective study conducted at Benha University hospital and National Heart Institute on one hundred patients undwent coronary artery bypass grafting (CABG) to evaluate the effect of CABG on the right ventricular (RV) function using speckle tracking echocardiography (STE). Methods: All cases were subjected to detailed medical history, full physical examination, 12 leads electrocardiogram (ECG), routine laboratory tests including (complete blood picture, liver functions, renal functions and lipid profile) and echocardiography either conventional echocardiography or STE, all parameters obtained before and within 2 weeks after surgery. Results: By conventional echocardiography there was statistically significant decrease in peak right ventricle systolic velociy (RVS) from (12.76 ± 1.72) to (7.33 ± 1.71) and tricuspid annular plane systolic excursion (TAPSE) from (22.8 ± 3.99) to (13.77 ± 4.63) among the studied patients after CABG. While there was significant increase in right ventricle fractional area change (RVFAC) from (44.69 ± 3.25) to (49.01 ± 3.36). On the other hand, there was non-significant change in right ventricle end diastolic diameter (RVEDD) at mid-cavity from (26.37 ± 2.72) to (26.53 ± 2.72) and basal segment from (36.05 ± 2.98) to (36.29 ± 3.04), right ventricle stroke volume (RVSV) from (65.44 ± 7.02) to (65.85 ± 6.86) and right myocardial performance index (RMPI) from (0.491 ± 0.088) to (0.498 ± 0.086). By STE There was statistically significant decrease in right ventricle global longitudinal strain (RVGLS) from (-20.63 to -14.1) after CABG. There was statistically significant decrease in right ventricle free wall longitudinal strain [apical decreased from (-23.73 to -13.7), mid-cavity decreased from (-25.76 to -11.53), basal decreased from (-20.39 to -10.13) and lateral wall declined from (-23.01 to -9.13)]. There was statistically significant decrease in interventricular septum longitudinal strain [apical decreased from (-19.77 to -10.06), mid-cavity decreased from (-17.81 to -10.87) and basal decreased from (-15.89 to -11.13)]. There was statistically significant increase in RV circumferential strain of lateral free wall from (-12.04 to -16.21), while there was non-significant change in RV circumferential strain of septum from (-19.77 ± 4.86) to (-20.37 ± 5.14). Conclusion: Distorted RV geometry after CABG can lead to altered deformation parameters, in other words longitudinal functional parameters may underestimate RV function and the decrease in RVGLS was compensated by increase in circumferential strain of lateral free wall of RV without change in RVSV or RMPI. Therefor changes in deformation parameters should always be interpreted in relation to change in geometry.

Permanent pacemaker implantation is conventionally done via upper limb veins. But in 1% - 6% cases, usual sub clavicular approach is either not possible or contraindicated due to complete occlusion of superior vena cava (SVC) or bilateral subclavian vein and/or bilateral implant site infection or thin skin [1]. Alternative approaches are warranted, including leadless pacemaker or complex lead extraction techniques, before considering surgical epicardial lead placement as a last resort because it has own hazards. We report a patient with complete heart block, total SVC obstruction, and a previously implanted malfunctioning epicardial lead presenting with pacemaker end of life. In view of exhaustion of the surgical option and in a resource constrained situation for lead extraction or leadless pacemaker, transiliac endocardial pacemaker implantation was done and a repeat surgery was averted. Learning objective: Complete venous occlusion is not very often encountered after pacemaker/ICD implantation. Apart from the risk of general anesthesia and invasive surgery, epicardial leads increase battery drain, and have a shorter operating life compared to an endocardial lead. The sparingly utilized iliac venous approach for permanent pacemaker implantation is a valuable, safe and minimally invasive alternative, when the conventional percutaneous access is unavailable, and surgery is undesirable or not possible. 

The involvement of the angiotensin II type 1 receptor in the Frank-Starling Law of the Heart, where the various activations are very limited, allows simple analysis of the kinase systems involved and thence extrapolation of the mechanism to that of angiotensin control of activation of cardiac and skeletal muscle contraction. The involvement of phosphorylation of the myosin light chain in the control of contraction is accepted but not fully understood. The involvement of troponin-I phosphorylation is also indicated but of unknown mechanism. There is no known signal for activation of myosin light chain kinase or Protein Kinase C-βII other than Ca2+/calmodulin but the former is constitutively active and thus has to be under control of a regulated inhibitor, the latter kinase may also be the same. Ca2+/calmodulin is not activated in Frank-Starling, i.e. there are no diastolic or systolic [Ca2+] changes. I suggest here that the regulated inhibition is by myosin light chain phosphatase and/or β-arrestin. Angiotensin activation, not involving G proteins. is by translocation of the β-arrestin from the sarcoplasm to the plasma membrane thus reducing its kinase inhibition action in the sarcoplasm. This reduced inhibition has been wrongly attributed to a mythical downstream agonist property of β-arrestin.

Biventricular (BiV) pacing revolutionized the heart failure management in patients with sinus rhythm and left bundle branch block; however, left ventricular-lead placement is not always technically possible. Also, BiV pacing does not fully normalize ventricular activation and, therefore, the ventricular resynchronization is imperfect. On the other hand, right ventricular pacing for bradycardia may cause or worsen heart failure in some patients by causing dyssynchronous ventricular activation. His bundle pacing comes as an alternative to current approaches as it activates the ventricles via the native His-Purkinje system, resulting in true physiological pacing, and, therefore, is a promising site for pacing in bradycardia and traditional CRT indications in cases where it can overcome left bundle branch block. Furthermore, it has the potential to open up new indications for pacing therapy in heart failure, such as targeting patients with PR prolongation, but a narrow QRS duration. In this article we explore the history, clinical evidence, proposed mechanisms, procedural characteristics, and the role in current therapy of His bundle pacing in the prevention and treatment of heart failure.

Background: Infants of diabetic mothers (IDMs) are at increased risk of developing congenital anomalies including cardiac defects. Pathological left ventricular hypertrophy, asymmetrical septal hypertrophy and outflow tract obstruction is a rare but known cardiac comorbidity in infants of diabetic mothers. The severity of this condition in IDMs can vary from an incidental finding on echocardiography to an infant with severe symptoms of congestive heart failure and specific management of the condition varies. Aim: The aim of this article is to report this clinical entity in a Nigerian infant born to a mother with poor glycaemic control in pregnancy and highlight management. Case report: We report a term neonate who was diagnosed as a case of pathological left ventricular hypertrophy, asymmetrical septal hypertrophy and outflow tract obstruction delivered to a mother with gestational diabetics with poor glycaemic control in pregnancy. Child was treated successfully with β-adrenergic blocker and showed resolution of hypertrophy in follow-up echocardiography. Conclusion: Infants of diabetic mothers are very high risk infants. Pathological left ventricular hypertrophy in IDM have good prognosis. Early recognition and prompt intervention is advocated.

Implantable cardioverter defibrillators (ICDs) are electronic devices that can prevent sudden cardiac death (SCD) caused by arrhythmic events in patients. The latest ESC/EAS and ACC/AHA Guidelines deem the placement of an ICDs appropriate in patients with heart failure class NYHA II and III in the presence of an ejection fraction less than or equal to 35% [1,2]. ICDs are usually not indicated in either class I or IV patients. The Guidelines recommendations for primary prevention of SCD with ICD implantation do not take into account the age of the patients but only their life expectancy which must be at least 1 year. Our patients usually are over eighty years old with heart failure and severely reduced ejection fraction. We must consequently decide if it is right to implant these patients with an ICD. Is the use of ICD in the patients over 80, in particular over 90 years old, really make sense becomes particularly important considering demographic changes that await us in the coming decades.

Background: Sudden cardiac death is a major healthcare issue in reduced ejection fraction heart failure (HFrEF) patients. Recently, the new association of sacubitril/valsartan showed a reduction of both ventricular arrhythmias (VA) and mortality even at low dose compared to enalapril in HF patients. The purpose of our study was to assess whether the highest dose of sacubitril/valsartan compared to lower doses may improve the rate of death and VA in a population of patients with HFrEF and with an implantable cardiac defibrillator (ICD). Methods: 104 HF patients with reduced EF under sacubitril/valsartan with an ICD were divided in 2 groups: the first one with the lower doses of sacubitril/valsartan (24/26 mg or 49 mg/51 mg twice daily) and the second with the maximal dose (97mg/103mg twice daily). The primary outcome was a composite of death or appropriate ICD therapy for VA. Results: After a median follow-up of 14 months, 39 patients were treated with lower doses and 65 patients with the highest dose. Patients from the lower doses group were older (70 [60-80] vs. 66 [60-70]; p = 0,03), more symptomatic at initiation (NYHA 3: 44% vs. 19%; p < 0,01) and more often in atrial fibrillation (31% vs. 12%; p = 0,04). The primary composite endpoint occurred in 14 patients (36%) in the low doses group versus 7 patients (11%) in high dose group (p < 0,01). This difference was particularly observed in the subgroup of patients with ischemic cardiomyopathy. In a multivariable analysis, the higher dose was independently associated with the primary outcome with an HR = 2,934 [IC 95% 1,147 – 7,504]; p = 0,03. Kaplan-Meier curve showed an early effect of the highest dose of sacubitril/valsartan association. Conclusion: Patients with HFrEF under the highest dose of sacubitril/valsartan showed better clinical outcomes with a decrease of both mortality or appropriated ICD therapies related to ventricular arrhythmias.

Peripartum cardiomyopathy is one of the curable cardiomyopathy. It’s a severe and frequent disease arising among women of childbearing age. Its evolution in the long-term among some patients leads to chronic heart failure. Our study aims to determine from a prospective cohort, the factors associated with the non-recovery of myocardial function upon 12 months of diagnosis. Sociodemographic, clinical and echocardiographic data were collected at the time of diagnosis and then in months 3, 6 and 12. The outcome was the non-recovery of myocardial function at one year, defined by a left ventricular ejection fraction (LVEF) below 50%. 60 patients were analyzed after 12 months of follow-up. Mortality was about 13.3% and recovery rate of myocardial function reached 42.3%. After logistic regression, delay diagnosis and observance were the factors related to non- recovery of myocardial function.

Desmodium adscendens is a rain forest medicinal herb used in managing quite a number of medical conditions. Its efficacy in the treatment of several diseases has made it a first line herb for doctors, especially in managing all forms of spasm. It is however common knowledge that some of these medicinal herbs impact severely on the normal functioning of some vital organs of the body during their administration. The present study was carried out to assess the renal and cardiovascular performance in subjects undergoing treatment with Desmodium adscendens with a view to advising against its indiscriminate use. The parameters used for the assessment of renal functions were serum creatinine and urea concentrations and their clearance. Also, changes in electrolyte concentration of Sodium, Potassium and Chloride concentration were used to assess cardiovascular performance. The histology of the kidney and heart tissues was also done to determine if the extract has impact on the cyto-architecture of the organs. Twenty-four (24) wistar rats were used for the experiment. The rats were grouped randomly into four groups (n = 6). Group 1 served as control, and the rats in the group were given normal rat feeds and water. Group 2 served as low dose group, and rats in this group were administered with low dose of extract 300 mg/kg. Group 3 served as medium group, and rats in this group were treated with medium dose of extract, 450 mg/kg. Group 4 served as high dose group, and rats in this group were treated with high dose of extract 600 mg/kg. The extract was administered for 28 days. Result showed that the extract did not impact negatively on the normal function of the renal and cardiovascular system of the treated groups, rather it enhanced their performances. It can therefore be concluded that the extract is beneficial to renal and cardiovascular functions if used within the treatment dosage. 

The normal adult heart is a well maintained machine that has a mechanism for growth replacement of the sarcomere that is lost by natural degeneration. This process ensures the heart has the strength of contraction to function correctly giving blood supply to the whole body. Some of the force of contraction of the sarcomere is transmitted to its major protein titin where its strength results in unfolding of a flexible section and release of a growth stimulant. The origin of all the cardiomyopathies can be traced to errors in this system resulting from mutations in a wide variety of the sarcomeric proteins. Too much or chronic tension transfer to titin giving increased growth resulting in hypertrophic cardiomyopathy (HCM) and too little leading to muscle wastage, dilated cardiomyopathy (DCM). HCM can ultimately lead to sudden cardiac death and DCM to heart failure. In this paper I show (1) a collection of the tension/ATPase calcium dependencies of cardiac myofibrils that define the mechanism of Ca2+ cooperativity. (2) I then reintroduce the stress/strain relationship to cardiomyopathies. (3) I then review the cardiomyopathy literature that contains similar Ca2+ dependency data to throw light on the mechanisms involved in generation of the types of myopathies from the mutations involved. In the review of cardiomyopathy there are two sections on mutations, the first dealing with those disrupting the Ca2+ cooperativity, i.e. the Hill coefficient of activation, leading to incomplete relaxation in diastole, chronic tension, and increased growth. Secondly dealing with those where the Ca2+ cooperativity is not affected giving either increased or decreased tension transfer to titin and changes in sarcomere growth. 

Background: Tetralogy of Fallot (TOF) is a very common cyanotic congenital heart disease presenting early at birth with various degrees of cyanosis. If left uncorrected surgically, can lead to death. Objectives: This study is aimed at determining pattern and surgical outcome of children with teratology of Fallot in a budding health facility in India over a year period. Result: A total of 51 children were diagnosed of TOF over the period, of which 66.7% were males with mean age of 48.14 ± 45.36 months. The surgical outcome showed only 3.9% mortality. The death was among children >1 to 5 years. The mean number of days in intensive care unit (ICU) was 5.8 ± 11.2 days. 82.4% of the patients were off-pump post-operatively, compared to 17.6% with re-pump. Among those who had re-pump, 77.8% were males and among those without re-pump, 64.3% were likewise males (χ2 = 0.6, p = 0.41). About 92.2% (47/51) of patients had pulmonary regurgitation post-op, ranging from mild to moderate regurgitation. 51.1% of the regurgitations were mild while 25.5% and 23.4% were moderate and severe regurgitations respectively. Post-operative VSD was detected in 51% (26/51) of the patients. The post-op right ventricular pressure (RVOT) was significantly lower than that of pre-op pressure, 10.8 ± 1.5 mmHg vs. 31.7 ± 4.5 mmHg (pair t test = 8.7, p < 0.001). Conclusion: Timely surgical repair is crucial in alleviating several morbidity and mortality associated with teratology of fallot. Pulmonary regurgitation is a very common sequel after surgery and can result in death.

With the discovery by Calghatgi (2013) that three common antibiotics (Abs) increased mitochondrial reactive oxygen (ROS) and lipid peroxide (LP) and depleted their natural absorbant glutathione led me to investigate further the potential impacts of these genotoxic substances on carcinogenesis. The range of impacts on mitochondria and cellular DNA varied by antibiotic to those consistent with known prior contributions to carcinogenesis. Specific cancers probably increased by these changes were HCC, RCC (KCC), CRC, cancer of the esophagus. Tumor suppressor gene mutations resulting from LP were noteworthy in this regard and mutations induced in CRC were consistent with those found in carcinogenesis of CRC. In addition depression of short chain fatty acids in microbiomes were found which depress the immune system increasing risk of all cancers. Many cancers were increased according to epidemiological studies linking Abs with elevated odds ratios, with one concern in particular, fatal breast cancer. The impact of loss of functionality of the mitochondria was also linked to depression of the citric acid cycle and therefore ATP which deflected metabolism to glycolysis, the Warburg mechanism also increasing risk of all cancers, favoured by cancer cells. In conclusion, some portion of many cancer types are probably increased in likelihood by number, type and frequency of Abs treatment and chronic residue exposure which varies from individual to individual. This led me to propose a three pronged carcinogenesis mechanism for Abs. 1. Cancer critical mutations 2. Immune depression 3. loss of mitochondrial functionality leading to Warburg effects. Damage to mitochondria were also noted by common pesticides tested in China and cancer associations were also found for many pesticides supporting a similar contributory etiology. Heart health concerns were raised by these findings because of the myriad mitochondria in the heart and because of long term reliability needs. Studies suggesting hearts were affected by Abs and pesticide exposure were presented. Because of their geographical ubiquitousness and the huge range of diseases associated with mitochondrial dysfunction, antibiotics and pesticides and bacteriocidal biocides are of concern for biodiversity and life in general. I propose research steps to evaluate Abs safety and suggest directions for further research and make suggestions on ways to ameliorate Abs toxicity.

Ventricular assist device is a portable machine which is also called an artificial heart for the patients who have terminal heart failure. The device maintains the heart’s vital functions until the suitable donor is found for the heart transplantation. It can be applied to either ventricles or both (biventricular). Although the device provides independence for the patient, it also has life-threatening complications. Such as infection, stroke secondary to thromboembolism, hemorrhage depending on anticoagulant use, right heart failure… and most of the time it is really hard to manage those complications. We will present a case, who had ischemic stroke as a complication of VAD even though he has been using aspirin, warfarin and had effective INR value.

Introduction: One of the major complications among COVID-19 patients include cardiac arrhythmias. Commonest arrhythmia is sinus tachycardia which is usually associated with palpitation causing discomfort to patients. In this study, we present a comparative study of use of Ivabradine vs. Carvedilol for sinus tachycardia in post-COVID-19 infected patients. Method: 50 consecutive recovered COVID-19 patients with sinus tachycardia were included in this open labelled RCT. 25 patients received Ivabradine and remaining 25 received Carvedilol. Single therapy non-responders were treated with Ivabradine with Atorvastatin. Results: The mean age of all patients is 48.8±7.66 years (Males 49.5 ± 7.21 years; Females 47.68 ± 8.23 years). The mean heart rate (MHR) of all patients is 125.52 ± 9.07/min (Males 125.67 ± 8.78/min; Females 125.26 ± 9.5/min). After five days of single drug therapy the mean drop in the heart rate was 35.04 ± 10.55/min (Males 34.41 ± 9.71/min; Females 36.05 ± 11.72/min), resulting in 27.88 ± 8.11% (Males 27.38 ± 7.56%; Females 28.69 ± 8.89%) reduction in MHR. Among the two groups, the Carvedilol group showed improvement of MHR in 14(56%) patients; whereas in Ivabradine group 18(72%) patients improved out of 25 patients each (p: 0.2385). In the Carvedilol group the MHR reduced from 128.6 ± 8.44 to 95.68 ± 10.63 (p < 0.001), which is statistically significant; similarly, the Ivabradine group showed a MHR from 122.44 ± 8.62 to 85.28 ± 10.52 (p < 0.001). The monotherapy therapy non-responders were treated with dual-therapy of (Ivabradine + Atorvastatin). Discussion: Ivabradine is more effective in controlling heart rate compared to Carvedilol. Also, Ivabradine group scores very well in ‘patient-satisfaction’ with regards to symptom (palpitation) relief. Conclusion: The COVID-19 sequelae of sinus tachycardia can be better controlled with Ivabradine when compared to Carvedilol.

Introduction: Atrioventricular nodal reentrant tachycardia (AVNRT) is the most frequent supraventricular tachycardia, commonly manifesting as autolimited paroxysmal episodes of rapid regular palpitations that exceed 150 beats per minute (bpm), dizziness and pounding neck sensation. Case presentation: We present a case of a male patient, 70 years old, with ischemic heart disease and slow-fast AVNRT treated with radiofrequency catheter ablation (RFCA) in March 2019, with regular 6-months follow-ups. He was readmitted in our department in November 2020 for rest dyspnea and incessant fluttering sensation in the neck, without palpitations. The event electrocardiogram (ECG) was initially interpreted by general cardiologist as accelerated junctional rhythm, 75 bpm. Due to the persistence of symptoms and ECG findings, a differential diagnosis between reentry and focal automaticity was imposed. The response to vagal maneuvers and Holter ECG monitoring characteristics provided valuable information. We suspected recurrent slow ventricular rate typical AVNRT, which was confirmed by electrophysiological study and we successfully performed the RFCA of the slow intranodal pathway. Conclusion: AV nodal reentry tachycardia may have an unusual presentation, occurring in elder male patients with structural heart disease. Antiarrhythmic drugs can promote reentry in this kind of patients. In cases of slow ventricular rate, vagal maneuvers and Holter ECG monitoring can help with the differential diagnosis. The arrhythmia can be successfully treated with RFCA with special caution regarding the risk of AV block.

Here I contrast the skeletal and cardiac muscle in terms of the control muscle growth and of sarcomere component synthesis. The differences are major and reflect the long term needs of the two systems. With the skeletal system there is growth of both the number of myocytes and the sarcomere components within them dependent on demand made of the muscle. Unlike skeletal muscles the normal adult heart is greatly restricted in size, number of myocytes and their content of contractile proteins, i.e. there is little change on demand. Over time proteins get damaged or decay and for the normal heart this implies a strictly controlled maintenance synthesis of sarcomere components. From the studies of abnormal, mutated systems there is one thing inherent to and more pronounced in cardiac muscle, the FrankStarling Law of the Heart derived from the angiotensin ii type 1 receptor that my studies indicate is central to the control of sarcomere component synthesis.

Sildenafil citrate is one of the frontline drugs used to manage erectile dysfunction (ED). Chemically, it is described as 1-[[3-(6,7-dihydro-1-methyl-7-oxo-3-propyl-1H –pyrazolo [4,3-d]pyrimidin-5-yl)-4 ethoxyphenyl] sulfonyl]-4-methylpiperazine citrate (C22H30N6O4 S). It is a highly selective inhibitor of cyclic guanine monophosphate-specific phosphodiesterase type-5. There had been heightened concerns following reports that sildenafil citrate may increase the risk of cardiovascular events, particularly fatal arrhythmias, in patients with cardiovascular disease. So the cardiac electrophysiological effects of sildenafil citrate have been investigated extensively in both animal and clinical studies. This article ties up the various outcomes of the investigations with a view to guiding physicians and patients that use sildenafil citrate to manage erectile dysfunction, especially as it concerns its effect on their cardiovascular function in health and in disease. Sildenafil citrate could impact negatively on ailing hearts, but on a healthy heart, there may not be any such impact, rather, it improves on heart performance as it lowers the blood pressure.