Dilated cardiomyopathy is a disease of the heart muscle that makes the muscle walls stretched and thin (dilated). The thinner walls are weakened, which means the heart can’t squeeze (contract) properly to pump blood to the rest of the body. The World Health Organization (WHO) defines dilated cardiomyopathy as a ventricular chamber exhibiting increased diastolic and systolic volume (left ventricular end-diastolic size > 115% of that calculated for age and body surface area) and a low (<40%) ejection fraction.

Dilated cardiomyopathy (DCM) occurs mostly in adults. It affects the heart’s ventricles and atria, the lower and upper chambers of the heart, respectively. Frequently, the disease starts in the left ventricle and the heart’s main pumping chamber. The heart muscle begins to dilate, meaning it stretch and become thinner. Consequently, the inside of the chamber enlarges. The problem often spreads to the right ventricle and then to the atria. As the heart chambers dilate, the heart muscle doesn’t contract normally and cannot pump blood very well. As the heart becomes weaker, heart failure can occur. Common symptoms of heart failure include shortness of breath, fatigue and swelling of the ankles, feet, legs, abdomen and veins in the neck. Dilated cardiomyopathy also can lead to heart valve problems, arrhythmias (irregular heartbeats) and blood clots in the heart. The exact cause of DCM is often unknown, although up to one-third of those affected inherit it from their parents. Some diseases, conditions and substances also can cause the disease such as coronary heart disease, heart attack, high blood pressure, diabetes, thyroid disease, viral hepatitis and HIV infections, especially viral infections that inflame the heart muscle. Peripartum cardiomyopathy as a complication during the last month of pregnancy or early months of birth can cause DCM. Certain toxins such as cobalt certain drugs (such as cocaine and amphetamines) and two medicines used to treat cancer (doxorubicin and daunorubicin) can cause DCM.

DCM is the most common cause of HF and a major health problem, even in young age groups, leading to disability. Many studies have been conducted worldwide, but to our knowledge, no such study has been done in Yemen. Therefore, we undertook this study to identify the most common risk factors associated with these diseases.

This study aimed to:

・ To determine the prevalence of DCM in heart failure patients in Dhamar Governorate, Yemen

・ To identify the risk factors associated with DCM among heart failure patients in Dhamar Governorate.

Dilated cardiomyopathy is defined by the presence of left ventricular dilatation and contractile dysfunction. Genetic mutations involving genes that encode cytoskeletal, sarcomere, and nuclear envelope proteins, among others, account for up to 35% of cases. Acquired causes include myocarditis and exposure to alcohol, drugs and toxins, and metabolic and endocrine disturbances. The most common presenting symptoms relate to congestive heart failure, but can also include circulatory collapse, arrhythmias, and thromboembolic events. Secondary neurohormonal changes contribute to reverse remodeling and ongoing myocyte damage. The prognosis is worst for individuals with the lowest ejection fractions or severe diastolic dysfunction. Treatment of chronic heart failure comprises medications that improve survival and reduce hospital admission―namely, angiotensin converting enzyme inhibitors and β blockers. Other interventions include enrolment in a multidisciplinary heart failure service, and device therapy for arrhythmia management and sudden death prevention. Patients who are refractory to medical therapy might benefit from mechanical circulatory support and heart transplantation. Treatment of preclinical disease and the potential role of stem-cell therapy are being investigated ‎[1] .

Cardiomyopathies are a heterogeneous group of myocardial diseases associated with mechanical or electrical dysfunction that usually exhibit inappropriate ventricular hypertrophy or dilatation [2] . Primary cardio myopathies are predominantly confined to heart muscle, whereas secondary cardiomyopathies are generally caused by systemic conditions with associated cardiac dysfunction. In the American Heart Association classification, cardiomyopathies are classified according to cause whereas the European Society of Cardiology classification is based on a combination of morphology and hemodynamics. Dilated cardiomyopathy is defined by the presence of left ventricular dilatation and contractile dysfunction, in the absence of abnormal loading conditions and severe coronary artery disease [3] [4] .

Dilated cardiomyopathy is one of the most common causes of heart failure and the most common indication for heart transplantation worldwide, with an estimated prevalence of 40 cases per 100,000 individuals and an annual incidence of 7 cases per 100,000 individuals [5] . Racial differences exist [3] [5] , whereas sex-related differences are less consistent [3] [6] . This disorder accounts for around 60% of childhood cardiomyopathies [7] [8] , with infants younger than 12 months having the highest incidence.

Genetic: causes are important at all ages. Clinical and echocardiographic screening in families of affected individuals shows evidence of familial transmission in 20% - 35% of cases [6] [9] [10] . Acquired causes of cardiomyopathy include infectious agents, drugs and toxins, and endocrine disturbances [1] . In children, common causes of dilated cardiomyopathy are genetic mutations, myocarditis, and inborn errors of metabolism [11] [12] .

Peripartum cardiomyopathy is defined by otherwise unexplained dilated cardiomyopathy, with onset in the last month of pregnancy or within 5 months of delivery [13] . Disease progression occurs in up to a half of cases and recovery occurs in less than a quarter. The fundamental cause is unknown and the highest incidence has been reported in sub-Saharan Africa [14] . In some cases, familial peripartum cardiomyopathy or familial dilated cardiomyopathy is present [15] . If heart function returns to normal, the risk of recurrence is low [16] .

Drugs and toxins: Alcohol abuse accounts for 21% - 36% of dilated cardiomyopathy cases in high-income countries [17] . The relationship between alcohol intake and clinical heart failure is influenced by various genetic, racial, and behavioral susceptibility factors [19] . The diagnosis is based on a history of heavy alcohol intake (>80 - 100 g/day for >10 years) [18] [19] , in combination with otherwise unexplained cardiomyopathy [20] . Cocaine and methamphetamines are potent sympathomimetic drugs that induce heightened inotropic and chronotropic effects. Mechanisms of cardiac toxicity include myocardial ischemia from increased oxygen consumption, prothrombotic effects, coronary vasospasm, and accelerated coronary atherosclerosis [21] [22] . The prevalence of methamphetamine abuse is high among young adult patients with newly diagnosed dilated cardiomyopathy [23] . Anthracycline-induced cardiotoxicity can occur during treatment or many years afterward. The mechanisms of anthracycline-induced cardiotoxicity include oxidative stress, changes in mitochondrial membrane permeability, and suppression of respiratory chain activity [24] [25] [26] . Echocardiographic abnormalities are detected in between 25% and 50% of childhood cancer survivors within 20 years of treatment. The cumulative risk of congestive heart failure 30 years after diagnosis is 8% in childhood cancer survivors who received a cumulative anthracycline dose of more than 250 mg/m² [27] [28] . Treatment with dexrazoxane, a free-radical scavenger, prior to anthracycline administration has been shown to diminish markers of acute myocardial damage [29] . The traditional histological criteria for myocarditis are based on an inflammatory cellular infiltrate, with or without myocyte necrosis [30] [31] [32] [33] . However, the clinical utility of these criteria is limited by both interobserver variability and low sensitivity; alternative criteria that rely on staining for various anti-CD surface antigens and antihuman leucocyte antigen might have greater sensitivity and improved prognostic value [30] [34] . Cardiac MRI can detect specific features of myocarditis without the sampling error associated with endomyocardial biopsy [35] [36] . The sequence of events leading to myocarditis typically starts with cardiac damage from viral infection (acute phase) resulting in exposure of intracellular antigens, leading to a T-lymphocyte-mediated inflammatory response (subacute phase). In some patients the inflammatory response can persist because of a misdirected immune response against endogenous heart antigens [30] . Myocarditis is an important cause of sudden death in adults younger than 35 years of age [37] and around 20% of patients with myocarditis develop a chronic dilated cardiomyopathy [38] . The typical manifestations of myocarditis are similar to those of dilated cardiomyopathy, but can vary from subclinical disease to arrhythmias, heart block, and sudden death, and can mimic myocardial infarction. In adults, fulminant lymphocytic myocarditis generally has a good prognosis [39] . Lymphocytic myocarditis accounts for around 10% of newly diagnosed adult-onset dilated cardiomyopathy, and is more common in children than adults. Myocarditis is most commonly caused by viral infection, although other infections can produce a similar clinical scenario [40] [41] . Coxsackievirus B, adenovirus, parvovirus B19, and human herpes virus 6 are common causes of myocarditis [41] [42] ; many other viruses have also been implicated.

Other forms of myocarditis are caused by drug-induced hypersensitivity and systemic hyper eosinophilic syndromes, whereas giant-cell my carditis is primarily autoimmune in nature.

Initial symptoms of heart failure are present in 80% of patients with dilated cardiomyopathy [43] . These symptoms include excessive sweating, ankle oedema, orthopnea, and fatigue after mild exertion. Abdominal discomfort, nausea, anorexia, and cachexia can be prominent in advanced cases. Circulatory collapse is the most severe manifestation of congestive heart failure. Some individuals have palpitations and syncope. Thromboembolic events and rarely, sudden death, might be the initial symptom, particularly in infants. Physical symptoms can include peripheral and sacral oedema, tachycardia, an elevated jugular venous pressure, pulmonary crepitations, an inferolateral displaced left ventricular apex beat, a gallop rhythm, and a mitral regurgitant murmur. Pathophysiology Left ventricular dilatation is accompanied by remodeling, in which the left ventricle assumes a spherical shape. Pathophysiological changes include a decrease in stroke volume and cardiac output, impaired ventricular filling, and an increase in end-diastolic pressure. Compensatory changes in the vascular system include an increase in systemic vascular resistance, a decrease in arterial compliance, and an increase in venous pressure and circulating blood volume. Both cardiac preload and afterload are increased, with increased afterload resulting in elevated wall stress [44] [45] . Diastole involves both active relaxation (early diastole) and passive compliance (mid-to-late diastole). In dilated cardiomyopathy, diastolic dysfunction that affects both components can accompany the reduction in systolic function. Impaired ventricular relaxation results in reduced rapid ventricular filling. Reduction in ventricular compliance due to hypertrophy or fibrosis causes restrictive pathophysiology, with reduced ventricular filling and elevated end-diastolic pressures. Secondary neurohormonal changes include an increase in sympathetic adrenergic activity and a reduction in vagal activity to the heart. Neurohormonal changes include an increase in circulating catecholamines, an increase in vasopressin levels, and activation of the renin-angiotensin-aldosterone system. Nature tic peptide production is also increased. The combination of increased catecholamines, increased cardiac afterload, fluid retention, and tachycardia result in further elevation of wall stress and myocardial oxygen demand, as well as direct cardiotoxicity [46] . These secondary adaptations lead to ongoing myocyte damage with further reduction in myocardial performance. Compensatory hypertrophy allows more muscle fibers to share in wall tension for any given ventricular pressure and radius.

The electrocardiogram (ECG) can only show non-specific repolarization abnormalities. Left ventricular hypertrophy, pathological Q waves, or poor R wave progression in the lateral chest leads might be observed. Prolongation of the PR interval might be the first manifestation of cardiomyopathy due to Lamin, emery, and SCN5A. Other abnormalities of conduction can mutations [47] [48] include atrioventricular block, left bundle branch block, and left anterior hemiblock. Chest radiographs usually show cardiomegaly and pulmonary venous redistribution, whereas pulmonary oedema is less common. Echocardiography typically shows global left ventricular hypokinesis; however, regional wall motion abnormalities might also exist. Left ventricular and atrial dilatation can be mild if the onset of the cardiomyopathy has been sudden. Right ventricular involvement is variable. Intracardiac thrombi and functional mitral regurgitation due to annular dilatation might also be noted. Doppler parameters can assist in quantifying the severity of diastolic dysfunction. Cardiac MRI provides accurate assessment of ventricular volumes, wall thickness, and contractile function, as well as tissue characterization. Delayed gadolinium enhancement can indicate myocardial necrosis or scarring. Myocardial inflammation is considered likely when necrosis or scarring (late gadolinium enhancement) is detected in conjunction with oedema (high signal T2 intensity) and hyperemia (early gadolinium enhancement) [49] [50] . The presence of a pericardial effusion supports the diagnosis of myocarditis [36] . Electrocardiography, tissue Doppler imaging [51] , and cardiac MRI can facilitate early detection of myocardial dysfunction in children with genetically determined cardiomyopathies, such as Duchenne muscular dystrophy, before the development of a typical dilated cardiomyopathy phenotype. Histological findings include irregular myocyte hypertrophy, with or without areas of fibrosis and myocyte damage. A lymphocytic infiltrate indicates the presence of inflammation that could be post-viral or immune mediated. Because of possible sampling error and variability in mechanisms of viral damage, the absence of these histological changes does not exclude the diagnosis of myocarditis. PCR can identify viral genome within the myocardium, even when inflammatory changes have resolved [41] . Cardiac histological examination can also help to identify specific disorders, such as sarcoidosis and haemochromatosis, and abnormal mitochondria, lysosomes, or myocardial inclusions, can indicate the presence of specific metabolic and storage disorders. Endomyocardial biopsy can be useful when a specific diagnosis is suspected that would influence therapy [52] [53] and is most helpful in patients with dilated cardiomyopathy who have recent onset of heart failure, ventricular arrhythmias, or Mobitz type II second or third degree atrioventricular heart block. Biomarkers, most commonly B-type natriuretic peptide (BNP) and N-terminal-BNP, are elevated in proportion to the severity of heart failure, leading to guidelines for their clinical use. In children with dilated cardiomyopathy, a BNP concentration greater than 300 pg/mL has been strongly associated with death, transplantation, or hospital admission due to heart failure.

Therapy of dilated cardiomyopathy is mainly directed at treatment of heart failure symptoms and prevention of disease progression and related complications, such as end organ dysfunction and stroke. Medical therapy remains the mainstay in patients with dilated cardiomyopathy and heart failure. Present oral regimen recommendations are outlined elsewhere [54] [55] , and have led to significant improvements in survival and symptom relief. In short, inhibition of angiotensin converting enzymes and β blockade with or without diuretics continue to be standard options. Treatment of decompensated heart failure is focused on diuresis with loop diuretics for volume overload and afterload reduction. Modulation of afterload can be accomplished with use of vasodilator therapy such as nitroglycerin, nitroprusside, or ebiratide. In patients with heart failure and clinical evidence of hypotension associated with hypoperfusion and raised filling pressures, intravenous inotropic support or vasopressor therapy, or both, should be considered. We prefer to avoid inotropes that increase mechanical stress, such as dopamine and dobutamine, in children, with milrinone continuing to be the most popular therapy. Once the need for other inotropic agents becomes clear because of deterioration in blood pressure and perfusion, we consider placement of an assist device. Some institutions use balloon pumps regularly in this instance. A comprehensive list of therapeutic strategies with supportive evidence is provided elsewhere [56] . Several clinical trials have assessed use of implantable cardioverter defibrillators in patients with low left ventricular ejection fractions, with results showing reduced mortality [57] [58] . For patients who have a left ventricular ejection fraction of less than 30% and symptomatic heart failure for which they are receiving optimum medical therapy, use of implantable cardioverter defibrillators is a class I indication, as outlined by the ACC/AHA guidelines. Treatment Therapy of dilated cardiomyopathy is mainly directed at treatment of heart failure symptoms and prevention of disease progression and related complications, such as end organ dysfunction and stroke.

Descriptive observational study design was conducted from Des 2021 to Jan 2022 at AL-Wahda Teaching Hospital and Taiba Consultative Hospital in Dahmer Governorate, Yemen

This study included:

・ Patient diagnosed to have HF.

・ Patient came with signs and symptoms of HF as (dyspnea, raise jugular venous pressure, congested hepatomegaly, bilateral basal lung crepitation, peripheral oedema).

This study excluded:

・ Patients who were asymptomatic.

・ Patients with severe renal or liver insufficiency.

・ Patient under 16-year-old.

This study was conducted at the Thamar University AL-Wahda Teaching Hospital (TUHTH) Mabar city and Taiba Consultative Hospital Dahmer Governorate, Yemen.

This study was carried out at the outpatient cardiological clinic and internal medicine department of TUHTH and Taiba Consultative Hospital.

Any patient diagnosed with heart failure in outpatient cardiological clinics or admitted to the Internal Medicine Department in AL-Wahda Teaching Hospital and Taiba Consultative Hospital during data collection period from Dec 2021 to Jan 2022 was included in this study, a total was 100 patients.

・ On a sheet, include demographic information (Age, Residence, Occupation, etc.).

・ The patient’s clinical data as etiological factors and information’s that pointed to risk factor as (smoking, obesity, hypertension, diabetes, and family history) all that were noted and record.

・ The results of the patient’s testing, including laboratory tests as (Renal function, lipid Profile, etc.) and other Investigation as (ECG, ECHO, Chest X-ray, etc.) were recorded.

Data processing, statistical analysis and graph drawing were performed using Statistical Package for Social Sciences (SPSS) (V.20.0)

・ The protocol of this study was approved by Thamar University Medical Ethics Committee (TUMEC NO 22006).

・ The consent was taken from patients before any examination, all of information was collected and kept strict confidently in order to follow the ethical and legal standards of the scientific investigate.

Attal of 100 patients with heart failure participated in this study according to our study most age group affected 42 (42)% were old age from (61 - 80 yrs.) and just 2 cases under 20-year, male mostly affected 61 (61%), married 91 (91%), 67 (67%) were from Dhamar city and half of the patients had duration of their illness of (1 - 5 yrs) 50 (50%). (Table 1)

When taking of medical history of patients most risk factors in our study in patients were Qat chewers 72 (72%), hypertension present in 60 (60%) of cases, (40%) were smoker. D.M. as a risk factor was in (32%) of patients, 29 (29%) of cases have family history of heart disease, history of CAD was found in 30 (30%), but pregnancy was found in only 2 case (2%). (Table 2)

Clinical features in Table 3 shows that most frequent symptoms was dyspnea in (96%), followed by lower limb oedema in 88(88%), then chest pain in 65 (65%) also palpitation was in 59 (59%), Rt. Hypochondrial pain in 54 (54%), syncopal attack 33 (33%) and less frequently abdominal distention in 30 (30%).

Physical examination in our study in patient with heart failure most patient have lower limb oedema in 86 (86%), congested neck vein in 73 (73%), crepitation 67 (67%), hepatomegaly 33 (33%), and less frequently ascites 23 (23%). (Table 4)

About laboratory investigation in our study, we did some investigations as CBC which was normal in most pts. 65 (65%) of cases, abnormal in 32 (32%) of cases and no data was present in only 3 (3%) of cases.

LFT no data was found in 79 (79%) of cases but in pts. Who did LFT 15 (15%) was normal and 6 (6%) was abnormal? RFT was normal in 65 (65%) of cases, but abnormal in 31 (31%) of cases and no data found in 4 (4%) of cases. Lipid profile no data found in 79 (79%) of cases among 21 case who did it 11 cases have abnormal and 10 cases have normal lipid profile. (Table 9)

In our study the radiological investigation was from the most important investigation we looked for to confirm the diagnosis of HF & DCM. In echocardiogram 100 (100%) of patients was abnormal, in ECG 4 cases only were normal, abnormal in 86 (86%) of cases but no data found in 10 (10%) of cases. In chest X-ray we found that the data was abnormal in 82 (82%) of cases, normal in 7 (7%) of cases and no data in 11 (11%) of cases. (Tables 10-12 and Figure 2)

Most patient treated by diuretics mostly loop diuretics and spironolactone also many patients treated by beta blockers 80 (80%) of cases and ACE inhibitors 72 (72%) of cases but few patients use the new drugs which are SGLT inhibitors 72 (72%) and ARNI 2 (2%) of cases mostly because they are expensive. (Table 13 and Figure 3)

This study could be concluded that dilated cardiomyopathy is the most common cause of HF (44%) similar to many studies worldwide. Dilated cardiomyopathy was more common in male than female and the major risk factor included was Qat chewing among Yemeni patients followed by hypertension and smoking. Also, pregnancy is a risk factor in 2 cases in our study.

From the findings of this study:

1) We recommend further studies in order to understand the exact cause and pathophysiology of DCM, determine the impact of them on clinical outcomes, identify effective treatments for their symptoms, and provide clinicians with the evidence for practical guidelines.

2) We need further studies to determine the effect of Qat chewing on cardiac diseases.

3) Educate the patients about the effect of bad habits such as Qat chewing and smoking on cardiac disease.

4) Educate the patient about the natural course of the disease and the importance of taking medication regularly.