Background: Pacemakers are an essential tool in managing bradyarrhythmias. Using the large Nationwide Inpatient Sample (NIS) database, we evaluated complications, trends and mortality rates of pacemakers over 2016 2020. Methods: We utilized International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) coding for our study. We evaluated clinical predictors, complications and mortality of pacemakers using the NIS database. Results: Significant independent Clinical predicators for pacer insertion are: NSTEMI: OR, 1.85; 95% CI, 1.80–1.91; p<0.001, hypertension: OR, 4.26; 95% CI, 4.19–4.34; p<0.001, hyperlipidemia: OR, 3.01; 95% CI, 2.97–3.05; p<0.001, atrial fibrillation/flutter: OR, 4.68 95% CI, 4.62–4.74; p<0.001, diabetes: OR, 1.49; 95% CI, 1.47–1.51; p<0.001, chronic kidney disease: OR, 1.99; 95% CI, 1.97–2.02; p<0.001, smoking: OR, 1.41; 95% CI, 1.31–1.43; p<0.001, COPD: OR, 1.11; 95% CI, 1.09–1.13; p<0.001, valvular heart disease: OR, 5.31; 95% CI, 5.21–5.41; p<0.001, systolic heart failure: OR, 1.98; 95% CI, 1.94–2.02; p<0.001, prior PCI: OR, 2.30; 95% CI, 2.26–2.34; p<0.001, obesity 1.19; 95% CI, 1.17–1.22; p<0.001), history of CABG{:OR, 2.48; 95% CI, 2.43–2.52; p<0.001, STEMI: OR, 1.86; 95% CI, 1.79–1.93; p<0.001, history of cardiomyopathy: OR, 1.90; 95% CI, 1.78–2.03; p<0.001, and endocarditis: OR, 1.77; 95% CI, 1.53–2.04; p<0.001. Pacemaker complication rates is around 2% Mortality around 1.44% Conclusion: We found many predictors for the need of pacemaker insertion. Mortality and complications have remained low over recent years.
IntroductionHypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular disease (1,2)  and is the most frequent cause of sudden cardiac death (SCD) in young individuals, particularly athletes with a high level of training (3–5).HCM is a prevalent hereditary cardiovascular condition that affects one in 500 people in the general population (6,7). The cumulative proportion of sudden cardiac death (SCD) events in childhood hypertrophic cardiomyopathy (HCM) within five years of diagnosis ranged from 8% to 10% (8,9). It is characterized by inadequate relaxation, hypercontractility, reduced compliance, and left ventricle hypertrophy (10–12). HCM manifests as a chronic, progressive illness that can have a severe, transformative effect on a person’s life and significantly lower quality of life. Data on the cost to society associated with HCM has shown significant increases in all-cause hospitalizations, hospital days, outpatient visits, and total healthcare costs. The majority of cost increases can be attributed to increased hospitalizations and hospital days among symptomatic patients (13). The most often reported symptoms include syncope, palpitations, exertional dyspnea, shortness of breath, ankle swelling, exhaustion, sense of disorientation, and lightheadedness (14,15).Among the estimated 700,000 patients with HCM, only 100,000 have been diagnosed in the United States (16). Underdiagnosis may be due in part to challenges in the diagnosis of asymptomatic HCM patients, who typically receive a diagnosis by chance or via systematic screening efforts (12). However, developments in the understanding of genetic and phenotypic characteristics of HCM have promise for improving the identification of the condition. Over the last twenty years, the condition has been linked to abnormalities in genes that encode proteins of the cardiomyocyte’s contractile machinery (6,17,18). It appears that significant progress has been made in understanding the illness from both a genetic and clinical standpoint (19).Despite new developments, HCM remains underdiagnosed. Although the population prevalence of HCM is between 1:200 and 1:500, only 10–20% of cases are found by clinical means (20). Patients with HCM can have a normal life expectancy but a notable percentage can develop HCM-related complications including heart failure, atrial fibrillation (AF), and cardioembolic stroke, while a smaller percentage have SCD or life-threatening ventricular arrhythmias (21). SCD is the most common cause of mortality among these patients and frequently occurs during exercise. However, it often goes undetected until death, as many individuals experience minimal or no significant symptoms (6,11). Consequently, a high index of diagnostic suspicion, accurate identification, and a thorough clinical examination of patients and family members are crucial for early identification and treatment (20). Identifying high-risk patients is crucial to lowering the risk of SCD in young individuals with HCM, as effective treatment has the potential to significantly reduce HCM mortality and morbidity (22,23) This can be achieved through exercise limitation, medication therapies, and the use of implantable cardioverter defibrillators (ICDs) (24) . Therefore, there has been considerable interest in improving diagnostic accuracy among HCM patients, especially young patients, to inform intervention (21).The HCM diagnosis is based on imaging techniques, such as echocardiography or cardiovascular magnetic resonance (CMR), that reveal increasing LV wall thickness (21). Thorough investigation has led to a better comprehension of risk categorization for patients with HCM. The latest European Society of Cardiology (ESC) guidelines propose evaluating clinical examination, family history, 48-hour electrocardiography (ECG), echocardiography, and exercise testing for this purpose (6,11). The European Society of Cardiology (ESC) has proposed specific cardiac screening guidelines for young competitive athletes (25), which include assessing symptoms and family medical history (e.g., premature death, HCM), conducting a physical examination, and performing a resting 12-lead ECG. A recent Danish study revealed that a large proportion of individuals who experienced SCD due to HCM had previous symptoms, and most of them had sought medical attention before their death, in contrast to the control group (26). These findings suggest there is an opportunity to improve the identification of HCM among at-risk patients, as many patients seek treatment.The ECG continues to be a fundamental aspect of evaluating patients with HCM. Moreover, it is experiencing a ”renaissance” in the realm of cardiomyopathies, not only due to its cost-effectiveness and widespread accessibility, but also because it offers information pertinent to morphology, function, and genetic foundation simultaneously (21) HCM has diagnosis so far relied on identification of left ventricular hypertrophy (LVH) with a wall thickness greater than 15 mm using echocardiography or CMR. However, this degree of LVH is not exclusive to HCM and may stem from various other pathological conditions, widening the differential. In such instances, the ECG is highly valuable in assisting with the differentiation between sarcomeric HCM and its phenocopies (21). There is a growing body of literature evaluating the accuracy of ECG markers in predicting HCM, however, there remains a need for research on the extent to which ECG findings are predictive of HCM identified on echocardiography. Therefore, the aim of this study was to evaluate the prevalence of abnormal ECG findings, including LVH, T wave inversion, left bundle branch block (LBBB), and left atrial enlargement in participants with suspected HCM detected during screening echocardiography.
Title: Occurrence of Low Diastolic Pressure and Cardiovascular Disease are More Common in Elderly that Could Explain Higher Mortality Rate in this populationMohammad Reza Movahed,1,2Department of Medicine, University of Arizona, Tucson, AZDepartment of Medicine, University of Arizona, Phoenix, AZCorrespondence to:Mohammad Reza Movahed, MD, PhDClinical Professor of MedicineCareMore Regional Director of Arizona7901 E SpeedwayTucson, AZ 85710Email: [email protected]: 949 400 0091Key words:Diastolic hypertension; hypertension; elderly; high blood pressure; cardiovascular risk factorConflict of interest: NoneLetter to Editor:With great interest, I read the paper entitled “Evaluation of Optimal Diastolic Blood Pressure (BP) Range Among Adults With Treated Systolic Blood Pressure Less Than 130 mmHg” by Li et al. (1) They found that diastolic BP less than 60 is associated with worse outcome in patients with age of over 50. (1) However, they have a major flaw in their data analysis as they did not adjust for age and any other risk factors in any multivariate analysis. We know that age is the most important factor for all cause or any mortality and hypertension rate increases with age. Patients with diastolic BP of < 60 in this study had much higher age that can clearly explain why this group had higher mortality. It is surprising that no multivariate adjustment was done in this study. As it can be seen from the table, mean age in patients with diastolic BP < 60 was 77.1 which was much higher than in other groups (66.9, 62.2 and 59.0). This is a very strong and highly significant difference. Looking at different age groups, I found similar issue with age cut offs. Patients with an age of <65 were only representing 23.1% of the population with diastolic BP <60 vs 44.8% in the next group of patients with diastolic BP between 60-70. Furthermore, not only they did not adjust their data for age, they also did not look at many other risk factors that are associated with hypertension needing adjustment. In large meta-analysis that was performed by Riaz et al. (2), they found that risk factors for hypertension includes smoking, obesity, diabetes mellitus, stress and anxiety which are all also risk factors for higher mortality. In their table, the authors document that the patients with diastolic BP of < 60 also had much higher significant history of cardiovascular disease as another unadjusted risk factor. Furthermore, they did not include other important risk factors commonly occuring in elderly such as presence of renal disease or chronic obstructive lung disease. I really hope that the authors will perform multivariate adjustment after reading this letter. Based on such a large difference in age distribution, we may not observe higher mortality rate in patients with diastolic BP of < 60 vs others after appropriate multivariate adjustment. Otherwise, the result of this study will be meaningless and very misleading.
Running Title: The Movahed Coronary Bifurcation Classification For LM bifurcationAuthors: Mohammad Reza Movahed, MD 1,2University of Arizona Sarver Heart Center, Tucson, Arizona,1 University of Arizona, Phoenix,2No Conflict of interestCorrespondent:M Reza Movahed, MD, PhD, FACP, FACC, FSCAIClinical Professor of MedicineUniversity of Arizona Sarver Heart Center1501 North Campbell AvenueTucson, AZ 85724Email: [email protected]: 949 400 0091Key words: Coronary bifurcation lesion; coronary bifurcation classification; Movahed classification; Movahed Bifurcation Classification; Bifurcation Intervention; Coronary Bifurcating lesionsConflict of interest: NoneWith great interest, I read the paper published in the JACC Intervention Journal entitled: “Provisional Strategy for Left Main Stem Bifurcation Disease: A State-of-the-Art Review of Technique and Outcomes “1 The authors used the Medina Bifurcation Classification that unfortunately divides true bifurcation lesions into three unnecessary groups: 111, 101 and 011. The authors should have used the Movahed classification which summarizes all true bifurcation lesions in one simple category called B 2 (B for bifurcation, 2 meaning both bifurcation ostia are diseased). The basic structure of the Movahed classification 2,3 simplifies bifurcation lesions into three categories: If both branches are involved as mentioned above, it is called a B2 lesion, if only the main branch is involved, is called B1m (B for bifurcation, 1m meaning only the main branch has disease) and if only side branch is involved, is called B1s lesion (B for bifurcation and 1s meaning only side branch has the disease). Another important part of this bifurcation classification is the fact that additional suffixes can be added if needed for clinical or research purposes. This comes in very handy, particularly in the left main bifurcation lesions. As the best example, the kissing stenting technique in appropriate bifurcation left main lesions can be performed very safely and quickly but it requires that the proximal segment be large enough to accommodate 2 stents and has to be at least 2/3 sum of distal bifurcation branches. In the Movahed classification, this suffix is called L (L for the large proximal segment) or S (for the small proximal segment). Furthermore, limitless additional suffixes can be added if needed such as calcium or bifurcation angle that is completely absent in the Medina classification.The widely used Medina bifurcation classification is unfortunately too complex in describing given true bifurcation lesions in three clinically irrelevant categories and at the same time lacks important other anatomical features of a given bifurcation lesion. 4-8 Figure 1 compares the basic structure of the Movahed classification to the Medina Classification. Figure 2 summarizes a detailed description of the Movahed classification if additional suffixes are needed.
Authors: Mohammad Reza Movahed, MD 1,2University of Arizona Sarver Heart Center, Tucson, Arizona,1 University of Arizona, Phoenix,2Correspondent:M Reza Movahed, MD, PhD, FACP, FACC, FSCAIClinical Professor of MedicineUniversity of Arizona Sarver Heart Center1501 North Campbell AvenueTucson, AZ 85724Email: [email protected]: 949 400 0091Key words: Percutaneous coronary intervention; stenting; balloon angioplasty: bifurcation lesion; acute coronary syndrome; acute myocardial infarction; unstable angina;PCIConflict of interest: NoneWith great interest, I read the paper entitled: “OCT or Angiography Guidance for PCI in Complex Bifurcation Lesions” published in the New England Journal of Medicine. (1) The Authors did a great job in randomizing patients to optical coherent tomography (OCT) vs. no OCT-guided bifurcation intervention. However, the most important anatomic features of a given bifurcation lesion were not mentioned and not studied at all. It is important that only true bifurcation lesions called B2 lesions (B for bifurcation, 2 meaning both ostia have significant disease) based on the Movahed bifurcation classification (2-4) needs a complex approach including the use of OCT. Not separating their bifurcation lesions into true vs. not true bifurcation lesions, they are not able to answer the simple questions: Do we really need OCT in non-true bifurcation lesions? Unfortunately, by not having any analysis of this important anatomical feature in this manuscript, the benefit of OCT remains uncertain for true or non-true lesions that could lead to under or overuse of OCT during bifurcation coronary interventions.
INTRODUCTION:Advanced chronic kidney disease is described as stages 3-5 of the chronic kidney disease classification defined as a reduction in glomerular filtration rate of less than 60 ml/min (1). Chronic kidney disease (CKD) has been known as one of the prominent risk factors for coronary artery disease (2). Percutaneous coronary intervention (PCI) has become an acceptable alternative to open heart surgery in patients suffering from coronary artery disease (3). This procedure improves patient survival, appropriately controls angina symptoms, reduces the need for long-term hospitalization, and reduces treatment costs (4-5). However, similar to other invasive or even minimally invasive therapeutic interventions, this procedure should be performed in high-risk groups with some considerations and precautions. These patients may experience far different outcomes than low-risk patients who have PCI. In patients with chronic kidney disorders, the need to use contrast material, scheduling consecutive dialysis sessions, the risk of microembolization, and requiring arterial wall instrumentation may lead to poorer outcomes of the PCI procedure, and the clinical benefits of PCI may be lower in such patients (6). In the last decade, various trials have evaluated the outcomes of the procedure in patients with CKD, which were basically associated with contradictory results. In a large, randomized trial (ISCHEMIA-CKD) on 777 CKD patients who underwent PCI procedure or medical therapy, 3.2-year outcomes including death, cardiac ischemic attack, or re-hospitalization were shown to be similar in both groups (7). In several trials, the presence of underlying chronic kidney disease was considered a major risk factor for long-term poorer outcomes following PCI, such as higher mortality and progression of renal impairment (8-9), also the impaired renal elimination of antithrombotic drugs exposes these patients to a higher likelihood of bleeding complications (10-11). During our literature review on databases, we found a small number of studies looking into the impacts of PCI on ACKD patients, Limpijankit and his colleague as one of the few studies in this matter determined one-year survival of PCI among 207 CKD patients stage 4-5 without dialysis and 5 with dialysis was 65.2%, 68.0% and 69.4 respectively (12).   Therefore, the outcome of PCI procedures in patients with ACKD still remains uncertain. In the present study, we investigated the clinical outcomes of PCI in cases with Advanced chronic kidney disease and compared the in-patient mortality rate of PCI between ACKD and non-ACKD candidates.
Background: The prevalence of hypertrophic cardiomyopathy (HCM) can be silent and can present with sudden death as the first manifestation of this disease. The goal of this study was to evaluate any association between reported physical symptoms with the presence of suspected HCM. Method: The Anthony Bates Foundation has been performing screening echocardiography across the United States for the prevention of sudden death since 2001. A total of 4,120 subjects between the ages of 6 and 79 underwent echocardiographic screening. We evaluated any association between any symptoms and suspected HCM defined as any left ventricular wall thickness ≥ 15 mm. Results: The total prevalence of suspected HCM in the entire study population was 1.1%. The presence of physical symptoms were not associated with HCM (chest pain in 4.3% of participant with HCM vs. 9.9% of the control, p=0.19, palpitation in 4.3% of participant with HCM vs. 7.3% of the control., p=0.41, shortness of breath in 6.4% of participant with HCM vs. 11.7% of the control., p=0.26, lightheadedness in 4.3% of participant with HCM vs. 13.1% of the control., p=0.07, ankle swelling in 2.1% of participant with HCM vs. 4.0% of the control., p=0.52, dizziness in 8.5% of participant with HCM vs. 12.2% of the control., p=0.44). Conclusion: Echocardiographic presence of suspected HCM is not associated with a higher prevalence of physical symptoms in the participants undergoing screening echocardiography. This finding confirmed that HCM can be asymptomatic in many patients and a questionnaire cannot distinguish the HCM population from a control group.